Best and Worst of Neuroscience and Neurology – May 2017

The latest from http://brainblogger.com!

What is genetic basis of our intelligence? How to stimulate deep areas of the brain? How to prevent Alzheimer’s disease?  How to slash the cost of treatment of multiple sclerosis? These are some of the questions highlighted in this monthly review of research literature. As usual, while we answer some questions, research studies also dispel some myths and assumption. Whether positive or negative,  the findings always help us to advance further our knowledge of brain and its abilities.

This month, we marked the birthday of Stanley Prusiner, the discoverer of prions – self-replicating proteins behind many neurodegenerative conditions such as Alzheimer’s disease and Parkinson’s disease. Recognising the importance of prions finally put the research aimed at finding the cure for these conditions on the right track.

 THE BEST

New genes for intelligence identified

Intelligence is highly heritable: it is estimated that 80% of our intelligence in adulthood is explained by genetic factors. However, our knowledge of specific genes involved in intelligence is very limited. New study published this month and based on the analysis of genetic data from 78,000 individuals reported 52 genes associated with intelligence, 40 of which are completely novel. Interestingly, many of these genes are also involved in determining other traits such as obesity, BMI, depressive syndromes, Alzheimer’s disease and others.

Brain region responsible for the fear of uncertain future is identified

Many people find it difficult to cope with an uncertain future. Surprisingly, it turned out that this particular behavioural feature closely relates to the size of one specific part of the brain – the striatum. New research suggests that a larger striatum is typically seen in people who have troubles dealing with uncertainties.  The study was done on psychologically healthy individuals, but an enlarged striatum has also been reported to be associated with general anxiety disorder and obsessive compulsive disorder.  Researchers speculate that an enlarged striatum may be linked to a higher risk of developing these disorders later in life.

Non-invasive method of stimulating deep parts of brain

Electric stimulation of deep parts of the brain has proven to be beneficial in treating a number of brain disorders, such as Parkinson’s disease, obsessive compulsive disorder, epilepsy, and depression. However, the approach requires implanting of an electrode directly inside the brain, which involves a risky and costly surgery. A new technique reported this month avoids this problem by using a pair of electrodes located on the surface of the scalp. The method relies on the use of a phenomenon known as temporal interference. This techniques allows the targeted delivery of electrical stimulation to deep areas of brain, such as hippocampus, without stimulating the surface brain area.

New cheap treatment for multiple sclerosis

Antibiotic minocycline, traditionally used as an acne medicine, may provide a safe new method of treating multiple sclerosis (MS), at a fraction of current cost of treating this disease. This drug was developed over 50 years ago. It attracted the attention of researchers studying MS due to its spectrum of anti-inflammatory activities. Phase III trials demonstrated that minocycline slows the progress of disease in patients diagnosed during the early stages of MS.

DNA-based vaccine for Alzheimer’s

Despite our growing understanding of the molecular mechanisms behind the development of Alzheimer’s disease, we still have no single treatment that could cure this condition or stop its progression. An earlier attempt to develop a vaccine preventing the development of Alzheimer’s disease has also failed due to severe side effects. However, new article published this month reports a new promising DNA-based vaccine that inhibits the accumulation of amyloid proteins in animals and shows no side effects observed in previous trials. It remains to be seen if these effects can be reproduced in humans.

Blood-brain barrier and omega-3 fatty acids

Omega-3 fatty acids are well known for their positive effects on general health. Recent findings demonstrate that these compounds are critical players in maintaining the integrity of the blood-brain barrier, the key structure for protecting the brain from various pathogens and toxins. Moreover, researchers demonstrated that permeability of the blood-brain barrier can be regulated by suppressing a protein that transports omega-3 acids to blood vessel cells. Making the barrier more penetrable is advantageous for efficient delivery of drugs when treating patients with various brain disorders.
THE WORST

No stress relief from high doses of tetrahydrocannabinol

Users of cannabis often claim that they use the drug for relaxation and stress relief. More detailed investigation of this effect shows a mixed picture. While experimenting with different doses of tetrahydrocannabinol (THC), the major active substance in marijuana, researchers found that small doses of the compound do indeed reduce stress. However, a slightly higher doses (sufficient to produce a mild “high”) produce an opposite effect and increase anxiety.

Visual cortex develops and matures much slower than assumed

It is traditionally believed that our visual system, including the parts of brain involved in the analysis of visual information, matures within the first few years of life. A new article published this month demonstrates that this assumption is incorrect. Visual cortex continues developing till the late 30s – early 40s. The authors of the article speculate that other parts of the brain may also reach maturity much later in life than currently assumed.

Transcranial direct-current stimulation  does not enhance cognitive training

Transcranial direct-current stimulation () is increasingly used as a method of improving learning abilities. The technique relies on passing weak electric impulses to the brain via electrodes attached to the scalp. Despite the growing popularity of this technique, the evidence in support of its advantages are very limited. A paper published this month casts further doubt on any benefits provided by tDCS. The author reported no improvements of working memory in a large group of subjects using this method, as compared to controls. Furthermore, the analysis of the existing literature on the subject also does not provide any meaningful support to the method. Clearly, further research on tDCS should be done to confirm or rule out the existence of its effects.

Poor sense of smell in humans is a misconception

The superiority of animals sense of smell compared to humans appears to be obvious to most people. After all, we do rely on a dog’s sense of smell for hunting, and it is well known how quickly sharks can detect the slightest smell of blood. However, a new article published this month in Science attempts to dispel the view that the human ability to detect smells is as bad as we are used to thinking. The number of brain cells involved in smell detection in humans is almost the same as in animals, and it is estimated that we can distinguish up to one trillion of different odors. We may lack the degree of specialization demonstrated by many animals in interpreting the information obtained through olfactory system, but the human ability to recognize smells is definitely much stronger than we are accustomed to think.

Women are not better than men at face recognition

It is commonly assumed that women are better  at recognizing and reading faces and correctly interpreting facial expressions. However, a study published this month casts serious doubts on this assumption. Using a series of tests, scientists demonstrated that no detectable difference in facial recognition exists between two genders. Importantly, the neuroimaging of the areas of brain known to be involved in face recognition has shown identical neural activity in both men and women when they were watching a video clip featuring multiple familiar and non-familiar faces.

References:

Suzanne Sniekers, Sven Stringer, Kyoko Watanabe, Philip R Jansen, Jonathan R I Coleman, Eva Krapohl, Erdogan Taskesen, Anke R Hammerschlag, Aysu Okbay, Delilah Zabaneh, Najaf Amin, Gerome Breen, David Cesarini, Christopher F Chabris, William G Iacono, M Arfan Ikram, Magnus Johannesson, Philipp Koellinger, James J Lee, Patrik K E Magnusson, Matt McGue, Mike B Miller, William E R Ollier, Antony Payton, Neil Pendleton, Robert Plomin, Cornelius A Rietveld, Henning Tiemeier, Cornelia M van Duijn, Danielle Posthuma. Genome-wide association meta-analysis of 78,308 individuals identifies new loci and genes influencing human intelligence. Nature Genetics, 2017; DOI: 10.1038/ng.3869

Justin Kim, PhD, Jin Shin, James Taylor, PhD, Alison Mattek, Samantha Chavez, and Paul Whalen, PhD. Intolerance of Uncertainty Predicts Increased Striatal Volume. Emotion, May 2017 DOI: 10.1037/emo0000331

Nir Grossman, David Bono, Nina Dedic, Suhasa B. Kodandaramaiah, Andrii Rudenko, Ho-Jun Suk, Antonino M. Cassara, Esra Neufeld, Niels Kuster, Li-Huei Tsai, Alvaro Pascual-Leone, Edward S. Boyden. Noninvasive Deep Brain Stimulation via Temporally Interfering Electric Fields. Cell, 2017; 169 (6): 1029 DOI: 10.1016/j.cell.2017.05.024

Luanne M. Metz, David K.B. Li, Anthony L. Traboulsee, Pierre Duquette, Misha Eliasziw, Graziela Cerchiaro, Jamie Greenfield, Andrew Riddehough, Michael Yeung, Marcelo Kremenchutzky, Galina Vorobeychik, Mark S. Freedman, Virender Bhan, Gregg Blevins, James J. Marriott, Francois Grand’Maison, Liesly Lee, Manon Thibault, Michael D. Hill, V. Wee Yong. Trial of Minocycline in a Clinically Isolated Syndrome of Multiple Sclerosis. New England Journal of Medicine, 2017; 376 (22): 2122 DOI: 10.1056/NEJMoa1608889

Doris Lambracht-Washington, Min Fu, Pat Frost, Roger N. Rosenberg. Evaluation of a DNA A?42 vaccine in adult rhesus monkeys (Macaca mulatta): antibody kinetics and immune profile after intradermal immunization with full-length DNA A?42 trimer. Alzheimer’s Research & Therapy, 2017; 9 (1) DOI: 10.1186/s13195-017-0257-7

Benjamin J. Andreone, Brian Wai Chow, Aleksandra Tata, Baptiste Lacoste, Ayal Ben-Zvi, Kevin Bullock, Amy A. Deik, David D. Ginty, Clary B. Clish, Chenghua Gu. Blood-Brain Barrier Permeability Is Regulated by Lipid Transport-Dependent Suppression of Caveolae-Mediated Transcytosis. Neuron, 2017; 94 (3): 581 DOI: 10.1016/j.neuron.2017.03.043

Emma Childs, Joseph A. Lutz, Harriet de Wit. Dose-related effects of delta-9-THC on emotional responses to acute psychosocial stress. Drug and Alcohol Dependence, 2017; DOI: 10.1016/j.drugalcdep.2017.03.030

Caitlin R. Siu, Simon P. Beshara, David G. Jones and Kathryn M. Murphy. Development of glutamatergic proteins in human visual cortex across the lifespan. Journal of Neuroscience, May 2017 DOI: 10.1523/JNEUROSCI.2304-16.2017

Jonna Nilsson, Alexander V. Lebedev, Anders Rydström, Martin Lövdén. Direct-Current Stimulation Does Little to Improve the Outcome of Working Memory Training in Older Adults. Psychological Science, 2017; 095679761769813 DOI: 10.1177/0956797617698139

John P. McGann. Poor human olfaction is a 19th-century myth. Science, 2017; 356 (6338): eaam7263 DOI: 10.1126/science.aam7263

Suzanne Scherf, Daniel B. Elbich, Natalie V. Motta-Mena. Investigating the Influence of Biological Sex on the Behavioral and Neural Basis of Face Recognition. eneuro, 2017; ENEURO.0104-17.2017 DOI: 10.1523/ENEURO.0104-17.2017

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The Neuroanatomy of Gossips

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We talk a lot. We are the only species on the planet that exchange information predominantly through talking. Other species, such as dolphins or primates, have their own languages, but they do not rely on verbal communication to the same degree, almost to the exclusion of other communication channels, as we do. Verbal communication is a cornerstone of our society. So what are we talking about so much? According to scientific research, we talk mostly about other people. In fact, a whopping two-thirds of our conversations consist of gossips. Of course, we discuss other things such as work, politics, sports, and weather, but overwhelmingly we talk about other people’s affairs, often not in a very positive light.

The scientific statistics on gossiping came as a surprise to me: what the intelligent, sensible and, as a rule, genuinely compassionate people around me would gain from spending so much time on gossips? I always believed that I almost never gossip. But when I tried to recall the topics of recent conversations with my friends, I have to admit that discussing other people does indeed take the lion’s share of what we talk about. Gossiping might be just a reflection of curiosity that all humans possess.

However, according to psychologists and evolutionary scientists, gossiping plays a key role in societal cohesion by spreading reputational information. The studies show that:

Individuals readily communicate reputational information about others, and recipients used this information to selectively interact with cooperative individuals and ostracize those who had behaved selfishly, which enabled group members to contribute to the public good with reduced threat of exploitation.

Thus, gossips mitigate egoistic behavior and counteract possible incentives to exploit the cooperative tendencies of others. They also serve to protect vulnerable members of society. Not bad!

The term “gossip” tends to have a negative connotation. Cambridge Dictionary defines gossip as conversation or reports about other people’s private lives that might be unkind, disapproving, or not true. Typically, the information shared via gossips is not substantiated by hard evidence. Although gossips are indeed often negative (and we will see below why we find negative gossiping more engaging), we do often talk about positive aspects of other people’s behavior too. We simply don’t view this kind of information sharing as gossiping. Negative gossiping might require a degree of secrecy (i.e., the subjects of the gossips are not informed about the fact that they were discussed – we talk about them behind their back). Unsurprisingly, people do not like when they find that they are being gossiped about, and hence there is a moral stigma attached to the people who are gossiping too much. However, more often than not, the gossips are not entirely negative – they tend to be a mixture of both positive and negative things. We provide other people with our assessment of another person’s reputation as we see it, typically involving both the person’s strengths and weaknesses, and with only limited evidence to substantiate either. These assessments might still be viewed unfavorably by the subjects of gossips, even when the assessment is predominantly positive. Nonetheless, we accept positive assessments with pleasure, but tend to be annoyed by criticism.

Being social creatures, we pay lots of attention to the opinion of others about us. Positive assessments by others are associated with higher social status, a larger number of friends and followers, and better chances of succeeding in any new venture and finding and attracting the best mating partners.

The part of the brain responsible for our social behavior is the prefrontal cortex. The prefrontal cortex is involved in social cognition and executive control. Social cognition refers to our ability to regulate our behavior and actions based on the real or assumed presence of other people. This is a trait that makes some want to conform to the norms and rules of society in which we live. Executive control channels our actual behavior and thoughts in the desirable direction. Studies with the use of functional MRI brain scans revealed the patterns of activation in the prefrontal cortex in response to positive and negative gossip about themselves, their best friends, and celebrities. A very interesting and revealing picture has emerged from these studies.

Two separate areas of the prefrontal cortex get activated in response to positive and negative gossip: positive gossip activates the orbital prefrontal cortex region, while negative gossip activates the superior medial prefrontal cortex. The intensity of responses was, however, very different depending on whether the gossip was about the subject of study or other people. Substantial activation of the superior medial prefrontal cortex was observed in both cases, regardless of the subject of the negative gossip. The orbital prefrontal cortex region was highly activated by positive gossip about the subjects themselves. However, this response was rather muted when the subjects listened to positive gossip about their friends or celebrities.

This study revealed volumes about the internal processes in our brain. It is quite clear that our ego makes us very attentive to any kind of information about ourselves passed around by other people. However, when it comes to information about others, we are biased to notice and register negative information preferentially. No wonder that the stories of scandals involving celebrities attract more attention than anything good these people do! Our own neuroanatomy makes celebrity magazines filled with the stories of scandals, cheating, and divorces, much more popular that magazines about happy family life.

References

Baumeister, R., Zhang, L., & Vohs, K. (2004). Gossip as cultural learning.(2), 111-121 DOI: 10.1037/1089-2680.8.2.111

Bosson, J. et al. (2006). Interpersonal chemistry through negativity: Bonding by sharing negative attitudes about others Personal Relationships, 13 (2), 135-150 DOI:10.1111/j.1475-6811.2006.00109.x

Dunbar, R. (2004). Gossip in evolutionary perspective. Review of General Psychology, 8 (2), 100-110 DOI:10.1037/1089-2680.8.2.100

Feinberg, M., Willer, R., & Schultz, M. (2014). Gossip and Ostracism Promote Cooperation in Groups Psychological Science, 25 (3), 656-664 DOI: 10.1177/0956797613510184

Feinberg, M., Willer, R., Stellar, J., & Keltner, D. (2012). The virtues of gossip: Reputational information sharing as prosocial behavior. Journal of Personality and Social Psychology, 102 (5), 1015-1030 DOI: 10.1037/a0026650

Martinescu, E., Janssen, O., & Nijstad, B. (2014). Tell Me the Gossip: The Self-Evaluative Function of Receiving Gossip About Others Personality and Social Psychology Bulletin, 40 (12), 1668-1680 DOI: 10.1177/0146167214554916

Peng X, Li Y, Wang P, Mo L, & Chen Q (2015). The ugly truth: negative gossip about celebrities and positive gossip about self entertain people in different ways. Social neuroscience, 10 (3), 320-36 PMID: 25580932

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Best and Worst of Neuroscience and Neurology – April 2017

The latest from http://brainblogger.com!

The number of neuroscience publications steadily grows over the years. In 2006, around 27,000 paper on this subject were published, while in 2015 this number went up to almost 37,000. This is a seriously big increase that reflects the importance of brain science and the growing interest in this field of research. The selection of articles presented here covers a wide range of topics, from purely academic subjects to the findings of clinical significance and newly discovered facts that will be of interest to almost everyone.

On the 25 April 1971, David Eagleman was celebrating his birthday. David is probably one of the best known neuroscientists these days, thanks to his books and TV series. In the academic world, Dr Eagleman is better known for hit works on the relationship between timing of perception and timing of neural signals.

THE BEST

New type of cells discovered in brain

This new discovery touches again on how little we still know about the brain. A new type of brain cell, mural lymphatic endothelial cells, were reported in the article published this week. The function of these cells, which are lymphatic in their origin, is to clean up the brain from accumulating cellular debris and thus prevent the damage to normal healthy cells of the brain.

Artificial synapse capable of learning

Brain synapses are central for our ability to learn. Stimulation of synapses strengthen the connection between the neurons and thus enhances the learning. A similar approach was used when researchers created an electronic synapse called memristor. Although the physical components of this nano-device have nothing to do with the real synapses in brain, the underlying principle is still the same. The devices of this kind will be important for the developing artificial brain.

Doxycycline for treating Parkinson’s disease?

Doxycycline has been used to treat bacterial infection for well over 50 years. New findings indicate that this antibiotic may have a new application: to treat Parkinson’s disease. This disease is caused by abnormal accumulation and toxicity of protein alpha-synuclein. In cell culture, the scientists observed that the formation of alpha-synuclein aggregates is reduced by 80% in the presence of doxycycline. Mice models with Parkinson’s disease fed on the diet with addition of doxycycline improved their symptoms. Human trials with low doses of doxycycline are now being planned.

Psychedelics and higher state of consciousness

The effects of psychedelics such as LSD on brain function are poorly studied. A paper published this month has reported that psychedelics induce increased signal diversity, as shown by brain imaging methods. Signal diversity is considered to be a measure of the complexity of brain activity. In the subjects exposed to the drugs, this measure was higher then the baseline value in the normal condition. Researchers conclude that, under the influence of psychedelics, the brain experiences a changed state of consciousness. The question remains whether this is a ‘better’ or more desirable state, and whether the psychedelic drugs can be used for therapeutic applications.

Growing brain tissue in a lab

Modelling the brain is very hard due to the complexity of this organ. While most other tissues and even organs can be grown in a laboratory artificially, the brain has resisted attempts thus far. A new paper published this month reported a successful attempt to do exactly this. Researchers successfully turned stem cells into tiny cultures of brain cells with several cell types typical for the midbrain. This is a very important methodological development that will help to facilitate the study of both the healthy brain and various brain pathologies.

THE WORST

Aspirin does not benefit cognitive functions

Aspirin is one of the oldest drugs still in use. Surprisingly, new beneficial qualities of this simple molecule are still being discovered. With only small and manageable side effects, low-dose aspirin is even recommended as a daily drug for older healthy individuals, for reducing the risk of serious conditions such as cardiovascular problems. There were many reports suggesting that aspirin might also be useful for protection against dementia and cognitive decline. However, the meta-analysis of existing data published this month found no evidence to support this view.

Soda drinking damages brain and accelerates its aging

The fact that sugary drinks are bad for general health is well known. New data based on a long-term study show that they are also damaging for brain functions. People consuming two or more sugary drinks at any time per day have poorer memory, decreased overall volume of the brain, and  a smaller hippocampus (a part of the brain associated with memory and learning). On the MRI scans their showed more prominent features of brain aging compared to people who don’t consume sugary beverages. Interestingly, switching to diet drinks containing artificial sweeteners doesn’t help much: people consuming at least one diet soda a day are three times more likely to develop dementia and stroke.

Marmite: bad choice for brain?

Marmite, a food spread popular in the UK, Australia, and New Zealand, might be not as safe and healthy as usually assumed. A rather curious piece of research published this month demonstrated that daily consumption of Marmite (one teaspoon every day) results in a 30% decrease in the brain response to visual stimuli. The effect is explained by the high content of vitamin B12 in Marmite. This vitamin regulates the level of neurotransmitter GABA that has an inhibitory effect on the excitability of some neurons. The findings show that the food we eat may have substantial effects on our brain functioning.

A link between cancer chemotherapy and depression

It was always difficult to figure out if the depression that cancer patients often experience is caused by the psychological stress of having cancer, or also because of chemotherapy. New research data obtained on healthy mice receiving drugs for brain cancer demonstrated that chemotherapy prevents formation of new cells in the hippocampus, a region of brain involved in memory formation and emotions. The treatment also resulted in the release of stress hormones and clear signs of depression. Brain cancer patients appear to be some of the most affected by the treatment-related depression, which remains mostly undiagnosed. Understanding that depression might be related to treatment will help to develop therapies to counteract this effect.

Multitasking: few advantages, brain overloading

The ability to multitask is often praised as a valuable skill, but does it really bring any advantages? New research data seriously questions the value of multitasking. Performing several tasks at the same task reduces productivity by 40%. Moreover, the findings show that frequent switching between tasks interferes with brain activity. Scientists also point out the danger of the continuous use of social media as it is an additional task for our brain and thus reduces the effectiveness of other tasks performed at the same time. It appears that focusing on a single task for a longer period of time brings better results than multitasking.

References:

Andy Wai Kan Yeung, Tazuko K. Goto, W. Keung Leung. The Changing Landscape of Neuroscience Research, 2006–2015: A Bibliometric Study. Frontiers in Neuroscience, 2017; 11 DOI: 10.3389/fnins.2017.00120

Neil I Bower, Katarzyna Koltowska, Cathy Pichol-Thievend, Isaac Virshup, Scott Paterson, Anne K Lagendijk, Weili Wang, Benjamin W Lindsey, Stephen J Bent, Sungmin Baek, Maria Rondon-Galeano, Daniel G Hurley, Naoki Mochizuki, Cas Simons, Mathias Francois, Christine A Wells, Jan Kaslin, Benjamin M Hogan. Mural lymphatic endothelial cells regulate meningeal angiogenesis in the zebrafish. Nature Neuroscience, 2017; DOI: 10.1038/nn.4558

Sören Boyn, Julie Grollier, Gwendal Lecerf, Bin Xu, Nicolas Locatelli, Stéphane Fusil, Stéphanie Girod, Cécile Carrétéro, Karin Garcia, Stéphane Xavier, Jean Tomas, Laurent Bellaiche, Manuel Bibes, Agnès Barthélémy, Sylvain Saïghi, Vincent Garcia. Learning through ferroelectric domain dynamics in solid-state synapses. Nature Communications, 2017; 8: 14736 DOI: 10.1038/NCOMMS14736

Florencia González-Lizárraga, Sergio B. Socías, César L. Ávila, Clarisa M. Torres-Bugeau, Leandro R. S. Barbosa, Andres Binolfi, Julia E. Sepúlveda-Díaz, Elaine Del-Bel, Claudio O. Fernandez, Dulce Papy-Garcia, Rosangela Itri, Rita Raisman-Vozari, Rosana N. Chehín. Repurposing doxycycline for synucleinopathies: remodelling of ?-synuclein oligomers towards non-toxic parallel beta-sheet structured species. Scientific Reports, 2017; 7: 41755 DOI: 10.1038/srep41755

Michael M. Schartner, Robin L. Carhart-Harris, Adam B. Barrett, Anil K. Seth, Suresh D. Muthukumaraswamy. Increased spontaneous MEG signal diversity for psychoactive doses of ketamine, LSD and psilocybin. Scientific Reports, 2017; 7: 46421 DOI: 10.1038/srep46421

Anna S. Monzel, Lisa M. Smits, Kathrin Hemmer, Siham Hachi, Edinson Lucumi Moreno, Thea van Wuellen, Javier Jarazo, Jonas Walter, Inga Brüggemann, Ibrahim Boussaad, Emanuel Berger, Ronan M.T. Fleming, Silvia Bolognin, Jens C. Schwamborn. Derivation of Human Midbrain-Specific Organoids from Neuroepithelial Stem Cells. Stem Cell Reports, 2017; DOI: 10.1016/j.stemcr.2017.03.010

Stubbs, Stefania Maggi, Trevor Thompson, Patricia Schofield, Christoph Muller, Ping-Tao Tseng, Pao-Yen Lin, André F. Carvalho, Marco Solmi. Low-Dose Aspirin Use and Cognitive Function in Older Age: A Systematic Review and Meta-analysis. Journal of the American Geriatrics Society, 2017; DOI: 10.1111/jgs.14883

Matthew P. Pase et al. Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia: A Prospective Cohort Study. Stroke, April 2017 DOI: 10.1161/STROKEAHA.116.016027

Matthew P. Pase, Jayandra J. Himali, Paul F. Jacques, Charles DeCarli, Claudia L. Satizabal, Hugo Aparicio, Ramachandran S. Vasan, Alexa S. Beiser, Sudha Seshadri. Sugary beverage intake and preclinical Alzheimer’s disease in the community. Alzheimer’s & Dementia, 2017; DOI: 10.1016/j.jalz.2017.01.024

Anika K Smith, Alex R Wade, Kirsty EH Penkman, Daniel H Baker. Dietary modulation of cortical excitation and inhibition. Journal of Psychopharmacology, 2017; 026988111769961 DOI: 10.1177/0269881117699613

M Egeland, C Guinaudie, A Du Preez, K Musaelyan, P A Zunszain, C Fernandes, C M Pariante, S Thuret. Depletion of adult neurogenesis using the chemotherapy drug temozolomide in mice induces behavioural and biological changes relevant to depression. Translational Psychiatry, 2017; 7 (4): e1101 DOI: 10.1038/tp.2017.68

Juha M. Lahnakoski, Iiro P. Jääskeläinen, Mikko Sams, Lauri Nummenmaa. Neural mechanisms for integrating consecutive and interleaved natural events. Human Brain Mapping, 2017; DOI: 10.1002/hbm.23591

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Does High Testosterone Mean Low Empathy?

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Empathy is defined as the ability to understand the feelings, emotions, and perspective of another person.  Empathy is critical for healthy social interactions, and impairments in empathy contribute to disorders of social interaction such as autism and psychopathy.

Women score higher on tests of empathy than men, leading researchers to examine a potential role for the male sex hormone testosterone in controlling empathy.  However, more recent studies have begun to explore the “dual hormone” hypothesis, that posits that testosterone interacts with the stress hormone cortisol to regulate social behaviours such as empathy.

A 2010 study by Jack van Honk and colleagues investigated the effects of acute testosterone administration on cognitive empathy in female volunteers. The study participants were administered either a placebo or a 0.5 mg dose of testosterone under the tongue, after which they took a test called, Reading the Mind in the Eyes Test (RMET).  This test measures how well an individual can interpret another’s emotions by reading expressions in the eye area of the face.

The participants took the test twice – once following administration of the placebo, and once after testosterone treatment – to assess how testosterone affected each subject individually.  Overall, the testosterone treatment reduced women’s scores on the RMET, suggesting that it impaired their ability to “read” the emotions and intentions of others through facial expressions in the eye area.

The researchers went one step further and measured the 2D:4D ratio of the study participants. This measure indicates the ratio in length between the index finger (second digit) and ring finger (fourth digit) and is considered a proxy measure of prenatal testosterone exposure.  Men have lower 2D:4D ratios than women, and women exposed to higher levels of testosterone in the womb display masculinized (lower) digit ratios. Elevated levels of foetal testosterone can occur in diseases such as congenital adrenal hyperplasia and polycystic ovary syndrome, and women with these disorders display reduced digit ratios. However, lower 2D:4D ratios are also found in otherwise healthy women due to individual variations in foetal hormone levels.

Van Honk et al. found that the RMET score reduction in response to testosterone was strongly correlated with the digit ratio, and that women with lower ratios (who thus had higher prenatal testosterone exposure) had stronger responses to testosterone.  These findings suggest an interesting “priming” effect of male hormone exposure during development that makes the brain more responsive to testosterone in adult life.

These findings provide support for the controversial ‘extreme male brain’ theory of autism, a disorder characterized by impairments in social interaction and a tendency to engage in repetitive behaviours. This theory posits that autism represents an extreme version of the normal male brain profile that is characterized by an increased systematizing ability and a reduced empathizing ability in comparison to females. The pathological impairment of empathy in autism may therefore arise from excessive “male” hormone levels during development.  Accordingly, reduced 2D:4D ratios have been observed in autistic individuals and in their first-degree relatives.

While this and other studies have demonstrated a clear inhibitory effect of testosterone on cognitive empathy, they tell only one part of the story. Other hormones may also play a role in the regulation of empathy.

One such hormone is cortisol, the body’s main stress hormone.  Cortisol and testosterone form the key players in the “dual-hormone hypothesis,” that seeks to explain how empathy, aggression, dominance, and other social behaviours are controlled by the brain.

A study by Zilioli et al. examined whether the levels of testosterone and cortisol in the blood were associated with empathy in a group of university students. The students took a series of tests that included the RMET as well as the Interpersonal Reactivity Index (IRI), a questionnaire designed to measure different aspects of empathy.  Saliva was collected for the analysis of cortisol and testosterone, and associations between hormone levels and RMET and IRI scores were assessed.

As predicted, testosterone levels were higher in men, and women scored higher on tests of empathy.  In women, there were no associations between hormone levels and empathy scores. However, an interesting association emerged between testosterone, cortisol and empathy in men, where an interaction between testosterone and cortisol was detected in relation to men’s IRI scores.

In men with higher than average testosterone levels, low cortisol predicted low empathy scores, whereas high cortisol predicted high empathy scores.  This association was not observed for men with testosterone levels below the mean, in whom cortisol showed no association with empathy.

In women, a similar pattern emerged when they were grouped according to testosterone levels: women with low cortisol and high testosterone had reduced empathy scores.  However, these differences did not meet the cut-off for statistical significance, probably due to the smaller number of women than men in the study.

A high testosterone, low cortisol profile has been linked with competitiveness and aggressive behaviour.  This profile has also been associated with psychopathy, a mental condition defined by anti-sociality, egotism, and impaired empathy.

In contrast, men with high testosterone levels and high cortisol in this study displayed increased empathy.  What are the implications for real life behaviour?

The researchers suggest that this profile could underlie certain altruistic behaviours such as acts of heroism where public safety is concerned.  They also posit that elevated cortisol levels might replicate a state of mild internal stress, which might be helpful for turning on feelings of empathy.

References

van Honk J, Schutter DJ, Bos PA, Kruijt AW, Lentjes EG, Baron-Cohen S (2011) Testosterone administration impairs cognitive empathy in women  depending on second-to-fourth digit ratio. Proc Natl Acad Sci USA. 108(8):3448-52. doi: 10.1073/pnas.1011891108

Peterson E, Miller SF (2012) The Eyes Test as a Measure of Individual Differences: How much of the Variance Reflects Verbal IQ? Front Psychol. 3:220. doi: 10.3389/fpsyg.2012.00220. eCollection 2012.

Baron-Cohen S (2002) The extreme male brain theory of autism. Trends Cogn Sci. 6(6):248-254. DOI: http://ift.tt/2qsiU5j

Zilioli, S., Ponzi, D., Henry, A. et al. (2015) Testosterone, Cortisol and Empathy: Evidence for the Dual-Hormone Hypothesis. Adaptive Human Behavior and Physiology 1: 421. doi:10.1007/s40750-014-0017-x

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Motor Neurons – Why Are They Important and How Are They Made?

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Motor neurons are the nerve cells in the body responsible for controlling movement.  A number of diseases are caused by damage to motor neurons, including amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA).  In order to treat these diseases, scientists are developing methods to generate new, healthy motor neurons from stem cells. A recent study has elucidated the cellular mechanisms that control the motor neuron differentiation, paving the way for new treatments for motor neuron diseases.

Each time we voluntarily move an arm or leg, or when our lungs involuntarily expand and contract, signals from the brain are sent along a chain to the spinal cord, where motor neuron cell bodies reside. These motor neurons terminate in muscle cells, where they transmit the nerve impulses in order to produce muscle contractions. In ALS, there is a progressive destruction of motor neurons due to either a genetic defect or an unknown environmental trigger. Motor neuron damage in ALS leads to progressive muscle weakness that affects all parts of the body, impairing the ability to speak, swallow, and eventually breathe. SMA is caused by gene mutations and is characterized by similarly progressive damage to motor neurons that causes muscle weakness. If respiratory muscles are affected, SMA can be fatal.

Scientists aim to develop gene therapies for these diseases that can repair the damaged motor neurons and improve the functioning and lifespan of patients. To do this, they must first understand the signals that induce motor neuron development from stem cells. Stem cells are the precursors for every type of cell in the body. They are triggered to differentiate into various cell types via cellular signaling molecules called transcription factors, which act on DNA to turn on specific genes. Which genes are turned on will determine the phenotypic fate of each cell. Typically, each cell goes through several stages of development before reaching its final fate.

A group of researchers from several universities recently teamed up to elucidate these programming pathways. They had previously discovered that a group of transcription factors called the NIL factors – Ngn2, Isl1, and Lhx3 – can induce motor neuron development from embryonic stem cells without passing through any of the intermediate stages. Moreover, the NIL factors achieved the transition to the motor neuron fate with a 90% success rate, and the process took only two days. This so-called direct programming pathway was an exciting finding with respect to clinical applications, because it can be achieved both in vitro and in living organisms at the site of cell damage.

In the current study published in the journal Cell Stem Cell, Esteban Mazzoni and colleagues further investigated the process by which transcription factors bind to and activate parts of DNA during the first 48 hours after NIL expression. First, the researchers used single-cell RNA sequencing (RNA-seq) to study the timing of gene expression after induction by NIL programming factors. RNA-seq is a technique that reveals the presence and quantity of RNA in a sample at a specific point in time. Thus, as transcription factors turn genes on, these genes are transcribed into RNA that can be measured and quantified.

The researchers also studied chromatin remodeling during motor neuron programming. Chromatin is a tightly-packed form of DNA which regulates the expression of genes through changes in its structure.  Promoters are regions of the DNA where transcription factors bind in order to initiate gene transcription.  Chromatin must undergo structural changes, called remodeling, in order for the DNA to be accessible to transcription factors. Typically, as cells move through the differentiation process, chromatin changes that occur at promoter regions will restrict the differentiation potential of the cell.

To study this chromatin remodeling process, a ChIP-seq time series was performed.  ChIP-seq combines chromatin immunoprecipitation with DNA sequencing to identify the binding sites of proteins that associate with DNA.  Antibodies against the bound proteins are used to extract protein-DNA complexes, and the DNA binding sites can be sequenced. In addition, the researchers used an assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) to study chromatin accessibility.  Proteins called transposons incorporate into exposed, or accessible, portions of chromatin. Therefore, identifying the locations of transposons in the DNA can indicate what parts of the DNA are being actively transcribed, or turned on.

This series of experiments revealed information about how genes are turned on and off over the 48-hour process of motor neuron formation.  Initially, the transcription factors Ngn2 and Isl1/Lhx3 induce different sets of genes in parallel. Whereas Ngn2 controls genes associated with generic neuronal differentiation, Isl1 and Lhx3  activate genes specific for spinal cord and motor neurons. As programming progresses, Ngn2 induces the expression of two other transcription factors, Ebf and Onecut. These transcription factors modify the chromatin state to enable Isl1/Lhx3 binding to previously inaccessible sites on the DNA that contain the terminal motor neuron genes necessary to complete the programming process.

These experiments showed that the activities of Ngn2 and Isl1/Lhx3 act in tandem to induce direct motor neuron programming from stem cells. The researchers hope to apply these findings clinically. By triggering this programming pathway in the body, cells in the spinal cord can be induced to differentiate into motor neurons, replacing the neurons that are damaged in diseases such as ALS.

References

Czarzasta J., Habich A., Siwek T., Czaplinski A., Maksymowicz W., Wojtikiewicz J. (2017) Stem cells for ALS: an overview of possible therapeutic approaches. Int J Dev Neurosci. DOI: 10.1016/j.ijdevneu.2017.01.003

Farrar M., Park S., Vucic S., Carey K., Turner B., Gillingwater T., Swoboda K., Kiernan M. (2016) Emerging therapies and challenges in Spinal Muscular Atrophy. Ann Neurol. DOI: 10.1002/ana.24864

Mazzoni, E.O., Mahony, S., Closser, M., Morrison, C.A., Nedelec, S., Williams, D.J., An, D., Gifford, D.K., and Wichterle, H. (2013). Synergistic binding of tran- scription factors to cell-specific enhancers programs motor neuron identity. Nat. Neurosci. 16:1219–1227. DOI:10.1038/nn.3467

Velasco S., Ibrahim M., Kakumanu A., Garipler G., Aydin B., Al-Sayegh M., Hirsekorn A., Abdul-Rahman F., Satija R., Ohler U., Mahony S., Mazzoni, E. (2016) A Multi-step Transcriptional and Chromatin State Cascade Underlies Motor Neuron Programming from Embryonic Stem Cells. Cell Stem Cell. DOI: 10.1016/j.stem.2016.11.006

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HIV Medications Linked to Increase in Alzheimer’s Disease Protein

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A class of drugs called protease inhibitors have been lifesaving for people with the human immunodeficiency virus (HIV). However, these medications come with a long list of side effects that may include impairments in cognitive function. How protease inhibitors might cause cognitive side effects has remained a mystery for some time. New research from the University of Pennsylvania is beginning to shed light on the answer, and it lies in a protein that is one of the main components of Alzheimer’s disease.

Protease inhibitors work to treat HIV by preventing replication of the HIV virus. The drugs block an enzyme called HIV protease, which cleaves the protein precursors required to produce new viral particles. Inhibiting HIV protease thus prevents the spread of the virus throughout the body. Since the approval of these drugs for clinical use in 1995, the rate of deaths from HIV has declined drastically. A typical HIV patient takes a combination of protease inhibitors and other medications to counter the development of drug-resistant HIV strains.

Side effects caused by protease inhibitors are common. These include dyslipidemia, hypercholesterolemia, metabolic syndrome, and, potentially, cognitive dysfunction. HIV-associated cognitive disorders, abbreviated HAND, include a spectrum of symptoms such as forgetfulness, confusion, and behavioral and motor changes. While the HIV virus itself is believed to play a role in causing HAND symptoms, the drugs used to treat the virus, including protease inhibitors, have also been implicated in the development of HAND. Until now, little was known about how protease inhibitors might cause cognitive side effects, and therefore, how such symptoms might be prevented.

Recent research from the University of Pennsylvania has shed new light on the mechanism by which protease inhibitors might impair cognitive function. Work by Kelly Jordan-Sciutto and colleagues in the Department of Pathology at the University of Pennsylvania has demonstrated that protease inhibitors increase levels of the peptide beta amyloid in the brain. Excessive levels of beta amyloid can impair the way brain cells function.

Beta amyloid protein is commonly known for playing a major role in Alzeheimer’s disease and several other neurological diseases, including Lewy body dementia, inclusion body myositis, and cerebral amyloid angiopathy. In Alzheimer’s disease, beta amyloid forms plaques or clumps of protein that give rise to deposits outside of brain cells, causing impairments in cell function. Increased levels of beta amyloid and its precursor protein – amyloid precursor protein (APP) – have also been observed in the brains of HIV-infected patients.

Jordan-Sciutto’s team had previously found that HIV drugs such as protease inhibitors can be toxic to neurons. They showed that some of these toxic effects were caused by damage to the DNA of the cell’s energy-generating cells, called mitochondria, which are located in the endoplasmic reticulum (ER). ER stress is known to activate the cell’s unfolded protein response (UPR) that increase the level of a protein called BACE1. In turn, BACE1 increases levels of beta amyloid by cleaving its precursor protein, APP.

Jordan-Sciutto theorized that because protease inhibitors cause ER stress, they might also increase beta amyloid by activating the UPR, and thus BACE1 and APP downstream. Their most recent study, published in the American Journal of Pathology, explored these questions further by examining whether protease inhibitors change the levels of beta amyloid and other cellular proteins that regulate its production.

To explore this question, a group of macaques were infected with the form of HIV found in monkeys, called simian immunodeficiency virus (SIV). Monkeys were then treated with either a cocktail of protease inhibitors or a placebo. The brains of the monkeys were examined 160 days following infection.

The results of the experiments showed that SIV-infected monkeys treated with protease inhibitors had much higher levels of beta amyloid in their neurons than infected monkeys who did not receive the drug. Infected drug-treated monkeys also showed increased levels of the amyloid beta precursor protein. As Jordan-Sciutto predicted, these monkeys also had increased levels of BACE1.

Interestingly, 90% of the placebo-treated animals developed signs of neurological dysfunction by 12 weeks of treatment, whereas the animals treated with the drug cocktail did not display any of these symptoms. This raises the question of whether the observed increases in amyloid beta protein in the drug-treated animals are pathological; that is, whether this amount of beta amyloid can cause symptoms. To date, the researchers have not studied monkeys treated with protease inhibitors in the absence of SIV infection in order to assess the effects of the drug alone.

To partly address this problem, the researchers also studied the effect of protease inhibitors on the unfolded protein response (UPR) in cultured cells derived from rat glial cells and human fetal tissue. Protease inhibitors increased the expression of markers associated with UPR activation and increased BACE1 in the cultured cells, which led to an increase in the cleavage of APP and subsequent cell damage. Conversely, treatment with a drug that inhibited BACE1 prevented this cell damage. Finally, the researchers showed that another enzyme, called PERK, was also a key player in the unfolded protein response that led to the increase in BACE1 levels.

These novel findings provide a clear mechanism for protease inhibitor brain toxicity in patients with HIV, suggesting that these drugs may in fact contribute to the development of HIV-associated cognitive disorders by increasing beta amyloid. Despite these neurotoxic effects, protease inhibitors will remain a mainstay for the treatment of HIV, as they have profoundly improved the quality of life and extended the lifespan of patients. The results of these studies suggest that potential new therapies targeting the proteins BACE1 and PERK could prevent the cognitive side effects of protease inhibitors.

References

Gannon, P., Akay-Espinoza, C., Yee A., Briand, L., Erickson, M., Gelman, B., Haughey, N., Zink, M. Clements, J., Kim, N., Van De Walle, G., Jensen, B., Vassar, R., Pierce, R., Gill, A., Kolson, D., Diehl, J. Mankowski, J., and Jordan-Sciutto, K. (2017) HIV Protease Inhibitors Alter Amyloid Precursor Protein Processing via ?-Site Amyloid Precursor Protein Cleaving Enzyme-1 Translational Up-Regulation. Am J Pathology. 187(1):91:109. DOI: http://ift.tt/2pTDL38

Gannon, P., Khan, M., Kolson, D. (2011) Current understanding of HIV-associated neurocognitive disorders pathogenesis. Curr Opin Neurol. 24(3):275-83. doi: 10.1097/WCO.0b013e32834695fb.

Green DA, Masliah E, Vinters HV, Beizai P, Moore DJ, Achim CL. (2005) Brain deposition of beta-amyloid is a common pathologic feature in HIV positive patients. AIDS. 19(4):407-11. PMID: 15750394

Giometto B, An SF, Groves M, Scaravilli T, Geddes JF, Miller R, Tavolato B, Beckett AA, Scaravilli F. (1997) Accumulation of beta-amyloid precursor protein in HIV encephalitis: relationship with neuropsychological abnormalities. Ann Neurol. 42(1):34-40.DOI:10.1002/ana.410420108

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Targeting Alzheimer’s: New Unorthodox Approaches

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Alzheimer’s disease affects an estimated 5 million individuals in the US and causes a devastating loss of cognitive function due to the buildup of beta-amyloid and tau proteins in the brain. Previous efforts to combat this disease have focused on developing drugs that target beta-amyloid, but such treatments have been unsuccessful in patients so far. Several exciting new approaches for treating Alzheimer’s are currently being tested in clinical trials in the US and Europe. These trials will assess the efficacy of an anti-viral drug that is normally used to treat herpes, and a new vaccine that generates antibodies against tau protein.

Alzheimer’s disease was first identified in 1906 and is the most common cause of dementia, responsible for an estimated 60–70 percent of dementia cases. Alzheimer’s predominantly affects the elderly, but approximately 5 percent of cases involve early-onset disease (prior to the age of 65). The predominant symptoms of Alzheimer’s are a loss of memory and other intellectual capacities, which must be severe enough to interfere with everyday functioning. Mood swings and behavioral difficulties are also predominant symptoms. As the disease progresses, motor functions can also be impacted, inhibiting the ability of patients to speak, swallow, and even walk. Affected individuals typically survive between 4–20 years beyond the time that their symptoms become noticeable to others, with an average survival time of 8 years.

Research into the causes of Alzheimer’s has revealed that two proteins, beta-amyloid and tau, play a key role in disrupting the neural processes that underlie memory and other cognitive abilities. Beta-amyloid normally acts to combat oxidative stress, regulate cholesterol transport, and fight off bacteria in the brain. In Alzheimer’s, however, beta-amyloid is overproduced. The excess protein forms clumps, or plaques, around neurons that can interfere with the transmission of nerve impulses. Tau is found in abundance in neurons and normally acts to stabilize cell proteins called microtubules in neuronal axons. In Alzheimer’s disease, defective forms of tau are produced, often containing large numbers of attached phosphate groups, termed hyperphosphorylated tau. Defective tau fails to stabilize microtubules, and instead binds together into insoluble aggregates or “tangles” of protein. The buildup of these neurofibrillary tangles inside of neurons, combined with amyloid plaques surrounding neurons, disrupts cell-to-cell communication in the brain.

Current therapies for Alzheimer’s include drugs that treat the symptoms of dementia by regulating neurotransmitter levels; however, none of these treatments directly addresses the cause of the disease. Research efforts have focused on finding a drug that can prevent the buildup of plaques by interfering with beta amyloid synthesis and aggregation. Unfortunately, despite promising preclinical data from animal studies, these drugs failed to produce results in humans or had devastating side effects. For example, one anti-beta-amyloid vaccine caused meningoencephalitis or inflammation of the brain tissue and surrounding membranes. This side effect may have resulted from the reaction of the vaccine with beta-amyloid normally present in the walls of blood vessels. Such serious side effects were cause for cessation of the trial, and researchers have subsequently turned their attention to other possible treatments.

A research team led by Hugo Lövheim from the Department of Community Medicine and Rehabilitation and the Unit of Geriatric Medicine at Umeå University in Sweden is piloting the first clinical study to address the effect of a herpes virus drug on Alzheimer’s disease. Lövheim’s group previously showed that infection with herpes virus was correlated with an increased risk of Alzheimer’s disease. People who tested positive for antibodies associated with the reactivated form of herpes simplex virus type 1 (HSV-1 anti-IgM) had double the risk of developing Alzheimer’s. Thus, the researchers surmised that brain signaling pathways activated by the virus might trigger the disease, and conversely, that anti-viral drugs might reverse disease symptoms.

The VALZ-Pilot study is currently recruiting participants with Alzheimer’s to investigate the effects of Valaciclovir, sold by the brand name Valtrex, a drug typically prescribed to treat genital herpes, cold sores, and shingles. Thirty-six participants will receive four weeks of drug treatment. Markers in the spinal fluid will be examined to assess the effect of the drug on several Alzheimer’s disease parameters, including levels of tau protein. A subset of subjects will also undergo positive emission tomography (PET) brain imaging analysis. By using a tracer that accumulates in cells with active herpes infection, this methodology can potentially detect this infection in the brains of Alzheimer’s patients.

A second new approach for treating Alzheimer’s, spearheaded by Petr Novak and colleagues at the Karolinska Institutet in Sweden, is the generation of a vaccine that targets the tau protein. Previous vaccine treatments for Alzheimer’s, which have thus far proven unsuccessful, focused only on beta-amyloid. The new vaccine, AADvac1, will prompt the body to generate antibodies against tau. The production of anti-tau antibodies will hopefully direct the immune system to clear tau protein from inside brain cells, similar to the way it fights off viruses and bacteria.

Developing a tau vaccine wasn’t easy; tau is a protein also found in healthy brains, and thus the removal of “healthy tau” by a vaccine could have negative side effects. The researchers compared differences in the structure of the healthy and pathological tau proteins, and identified what they call the “Achilles heel” of the abnormal protein. They were then able to create a vaccine that recognizes this feature of the abnormal protein, yielding treatment specificity for the disease-causing tau.

So far the AADvac1 vaccine is in phase 1 of clinical trials, which involves administration of the drug to healthy volunteers to assess side effects, but does not address efficacy. No serious side effects have been observed thus far, and volunteers have experienced only minor reactions at the injection site, similar to other types of vaccines. The lack of side effects is a promising first step. Moreover, the trial has also demonstrated the effectiveness of the drug to elicit an immune response, which is a critical factor for its success. These promising preliminary data provide much-needed hope for Alzheimer’s patients and their families.

References

Hippius H, Neundörfer G. (2003) The discovery of Alzheimer’s disease. Dialogues Clin Neurosci. 5(1):101-8. PMID: 22034141.

Marciani D. (2016) A retrospective analysis of the Alzheimer’s disease vaccine progress – The critical need for new development strategies. J Neurochem. 137(5):687-700. doi: 10.1111/jnc.13608.

Novak P, RSchmidt R, Kontsekova E, Zilka N, Kovacech B, Skrabana R, Vince-Kazmerova Z, Katina S, Fialova L, Prcina M, Parrak V, Dal-Bianco P, Brunner M, Staffen W, Rainer M, Ondrus M, Ropele S, Smisek M, Sivak R, Winblad B, Novak M. (2016) Safety and immunogenicity of the tau vaccine AADvac1 in patients with Alzheimer’s disease: a randomised, double-blind, placebo-controlled, phase 1 trial. The Lancet Neurology. S1474-4422(16)30331-3. doi: 10.1016/S1474-4422(16)30331-3.

Lövheim H, Gilthorpe J, Adolfsson R, Nilsson L, Elgh F. (2014) Reactivated herpes simplex infection increases the risk of Alzheimer’s disease. Alzheimers Dement. 11(6):593-9. doi: 10.1016/j.jalz.2014.04.522.

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