New Target in Brain for Treating Depression — The BMP Pathway

A significant number of patients do not respond to antidepressant drugs, and some even feel worse, a somber fact that emphasizes the urgent need to find other treatment options.

In a new study on mice, scientists at Northwestern Medicine have discovered a pathway in the brain that may be a promising new drug target for people with non-responsive depression.

Sarah Brooker, the first author and an M.D./Ph.D student at Northwestern University Feinberg School of Medicine explains:

Identifying new pathways that can be targeted for drug design is an important step forward in improving the treatment of depressive disorders

Brooker conducted the study in the lab of senior study author Dr. Jack Kessler, a professor of neurology at Feinberg and a Northwestern Medicine neurologist.

The aim of their research is to gain a better understanding of how current antidepressants work in the brain, with the ultimate goal of finding new drug targets that are more effective for people who do not respond to current medications.

During the study, scientists discovered for the first time that antidepressant drugs such as Prozac and tricyclics target a pathway in the hippocampus called the BMP signaling pathway. A signaling pathway is a group of molecules in a cell that work together to control one or more cell functions.

Like a cascade, after the first molecule in a pathway receives a signal, it activates another molecule and so forth until the cell function is carried out.

The researchers found that Prozac and tricyclics inhibit this pathway and, thereby, trigger stem cells in the brain to produce more neurons responsible for mood and memory formation. However, the researchers didn’t know if blocking the pathway contributed to the drugs’ antidepressant effect because Prozac acts on multiple mechanisms in the brain.

After confirming the importance of the BMP pathway in depression, the scientists investigated a brain protein, called Noggin, on depressed mice. Noggin is known to block the BMP pathway and stimulate new neurons, a process known as neurogenesis.

They discovered Noggin blocks the pathway more precisely and effectively than Prozac or tricyclics, as the mice soon experienced a strong antidepressant effect.

A sign of depression in mice is a tendency to hang lifelessly when held by the tail, rather than struggle to get themselves upright. After receiving Noggin, mice energetically tried to lift themselves up, whereas control mice were more likely to give up and just hang there.

The mice were then placed in a maze with secluded (safe) and open (less safe) spaces. The Noggin mice were less anxious and explored more mazes than the control mice.

As put by Kessler, also the Ken and Ruth Davee Professor of Stem Cell Biology:

The biochemical changes in the brain that lead to depression are not well understood, and many patients fail to respond to currently available drugs. Our findings may not only help to understand the causes of depression, but also may provide a new biochemical target for developing more effective therapies.

This guest article originally appeared on Scientists Target New Pathway in Brain to Alleviate Depression


Brooker, S. M., Gobeske, K. T., Chen, J., Peng, C.-Y., &038; Kessler, J. A. (2016). Molecular psychiatry &8211; abstract of article: Hippocampal bone morphogenetic protein signaling mediates behavioral effects of antidepressant treatment. Molecular Psychiatry. doi:10.1038/mp.2016.160

Image via geralt / Pixabay.

“I’ll Do It Later” – Brain Connectivity Predicts Procrastination

Procrastination — we are all guilty of it. Irrationally delaying a task in day-to-day life can have minor effects, such as lost sleep from staying up late to meet a deadline, but it can also be detrimental. From a health perspective, waiting to go to the doctor until an illness becomes severe could be fatal. In the financial domain, procrastinating on taxes costs people hundreds of dollars per year in overpayments, and failing to start saving early for retirement can end up costing thousands of dollars. So why do we procrastinate, even though we know it is bad for us? There is a common perception that procrastination is associated with laziness or lack of motivation, but a recent fMRI study suggests something else.

A recent study published in Personality and Individual Differences by Wu and colleagues provides some insight into the neural underpinnings of procrastination by looking at a specific type of brain connectivity, resting state functional connectivity (rsFC), and investigating how this relates to individual levels of procrastination. This approach looks at how different regions of the brain are functionally connected, as opposed to anatomically (structurally) connected. When the brain is at “rest”, there is still some activity going on; it is always spontaneously firing at low-frequency fluctuations. Recent research has shown that there are distinct brain networks that fire together at rest, and these patterns have been linked to variations in cognitive abilities and behaviors.

The researchers hypothesized that procrastination is a result of failure in self-regulation, and thus brain regions involving impulsivity control and self-monitoring may have less functional connectivity in individuals who procrastinate more. They used measures of trait procrastination and self-control to assess procrastination tendencies and collected resting state fMRI data during which participants were instructed to lie quietly in the scanner, close their eyes, and let their mind wander for about 6 minutes. After careful analysis, Wu and colleagues were able to confirm that the functional connectivity between the hypothesized brain regions were indeed related to procrastination behavior. The circuit between the ventromedial prefrontal cortex, an area associated with value comparison, and the dorsolateral prefrontal cortex, a region involved in the control of behavior, was found to have reduced connectivity in high procrastinators. Similarly, the connectivity between the dorsal anterior cingulate cortex, involved in cognitive control, and the caudate, a reward processing area of the brain, was also reduced in severe procrastinators. Finally, the researchers evaluated connectivity within the ventrolateral prefrontal cortex, an area responsible for behavioral inhibition, and found that this was reduced in heavy procrastinators as well.

When they put everything together, as they expected, the behavioral measure of self-control was the best predictor of procrastination tendencies, but the neural functional connectivity was actually able to add significant additional predictive power on top of what self-control could predict by itself. This suggests that there is something unique about the neural connectivity that is able to predict procrastination beyond the self- control that is measured in the lab. The reduced functional connectivity in high procrastinators observed in regions of their brains suggest that procrastination is related to other factors linked to self-control, such as impulse control inability and optimal weighting of value options, something that has only been speculated by researchers before.

So, how does this information help researchers figure out ways to help people reduce procrastination? Identifying that procrastination is associated with a lack of self-control and impulsivity provides a good starting point for interventions that may reduce that behavior. A review by Piers Steel at University of Calgary suggests that procrastination might be reduced by increasing one’s confidence about completing a task, reducing distractions, fostering automaticity by creating habits, and setting daily goals. There has also been a recent interest in internet-based cognitive behavioral therapy. Rozental and colleagues at Stockholm University created an online based 8-week treatment program with different modules designed to reduce procrastination, with topics such as goal-setting, time management, and motivation. In a study of 150 participants who all scored extremely high (top 25%) on an index of procrastination behaviors, they found that internet-based cognitive behavior therapy was able to substantially improve self-report difficulties with procrastination in participants who completed the modules in comparison to control participants who did not complete the treatment, demonstrating that online training can indeed be effective for even the worst procrastinators.

One thing is for sure: the recognition of procrastination as a cognitive deficit is increasing. All of this work provides a promising start for awareness and treatments for even the most severe procrastinators.


  1. Steel, P. The nature of procrastination: a meta-analytic and theoretical review of quintessential self-regulatory failure. Psychol. Bull. 133, 65–94 (2007). DOI: 10.1037/0033-2909.133.1.65
  1. Wu, Y., Li, L., Yuan, B. & Tian, X. Individual differences in resting-state functional connectivity predict procrastination. Pers. Individ. Dif. 95, 62–67 (2016). DOI: 10.1016/j.paid.2016.02.016
  1. Rozental, A., Forsell, E., Svensson, A., Andersson, G. & Carlbring, P. Internet-Based Cognitive Behavior Therapy for Procrastination: A Randomized Controlled Trial. JMIR Res. Protoc. 83, 808–824 (2015). DOI: 10.1037/ccp0000023

Image via Comfreak / Pixabay.

Best and Worst of Neuroscience and Neurology – August 2016

This article summarizes some interesting publications that came out in August. As usual, there were many interesting developments, both in fundamental neuroscience and neurology, and in practical aspects of dealing with and treating brain-related diseases and disorders.

On August 20, the scientific community marked the birthday of Roger Sperry. Prof. Sperry received the 1981 Nobel Prize for Medicine and Physiology for his works on “split-brain” patients. In these patients, the corpus callosum connecting two brain hemispheres is severed. The works of Roger Sperry helped to establish that our two brain hemispheres do have different functions and often work independently.


Brain maintains representation of amputated hand decades later

It was traditionally assumed that after amputation of a hand or a finger the part of the brain representing it becomes “overwritten” due to the absence of input signals. New data demonstrate that this view is not correct and brain retains the picture of missing limb even several decade later. The findings might prove useful in creating neuroprosthetics – artificial limbs controlled directly by brain signals.

New blood test predicts the likelihood of developing Alzheimer’s disease in the future

Although early Alzheimer’s disease often manifests itself as a mild memory impairment, only some of patients with memory impairment will eventually develop this condition. New blood test developed by British scientists allows to predict the likelihood of developing the Alzheimer’s in the next few years in patients with mild memory problems. The test would help to identify vulnerable patients and advise them early on the course of action to prevent or delay the disease progression.

Parkinson’s disease spreads via intercellular nanotubes

Like most other neurodegenerative diseases, Parkinson’s disease is linked to formation and spread of protein aggregates, alpha-synuclein in the case of this condition. However, not much is known about the mechanisms responsible for the transfer of protein aggregates between the neural cells in brain. This month, researchers reported that alpha-synuclein aggregates can migrate from one cell to another along tunnelling nanotubes. The findings represent a serious breakthrough in understanding Parkinson’s disease and point to some new potentially useful therapeutic targets.

Lead causes oxidative stress in neural stem cells

Environmental exposure to lead is known to cause neurodevelopmental problems, particularly at early stages of life. The molecular mechanisms behind this effect remained unclear, however. Now scientists have found that lead induces oxidative stress in neural stem cells. Specifically, proteins SPP1 and NRF2 were found to be involved in this process. Both proteins are involved in cognitive development.

Genetic reprogramming can convert connective tissue cells into neurons

Genetic reprogramming of mature cells to create pluripotent stem cells was discovered 10 years ago. A number of improved technics for cellular reprogramming was invented since then. A novel revolutionary technique called CRISPR was recently used to convert the cells of connective tissue into neurons. The discovery may pave the way to model neurological disorders and develop cell therapy.



Stopping exercise at older age leads to decreased cerebral blood flow

The fact that fitness level drops quite quickly after stopping exercise is well known, but the changes in brain caused by termination of the regular exercise routine are not well studied. In a new research, scientists asked well trained senior athletes aged 50-80 years to stop exercising for 10 days, and then studied their cerebral blood flow. It turned out that all athletes experienced significantly decreased level of resting blood flow in a number of key areas of brain. Importantly, the blood flow was decreased in hippocampus, a part of brain crucial for learning and memory. Researchers believe that stopping exercise at older age may trigger the processes connected to the development of dementia and other neurodegenerative conditions.

Larger brain, not different brain structure, differentiates us from primates

For a long time, scientists believed that our remarkable cognitive abilities are linked to the enlarged prefrontal cortex region of the brain. As the new article published this month shows, this idea was wrong. In both humans and non-human primates, the prefrontal cortex occupies 8% of the brain. Human brain, however, is much bigger and contains 16 billion cortical neurons, while other higher primates have only 6-9 billion of these cells. Apparently, this increased number of neurons, rather than larger prefrontal cortex, is behind our enhanced cognitive abilities.

Calcium supplements increase risk of dementia in women with history of stroke

Osteoporosis is a common problem in elderly women, and calcium supplementation is usually recommended to manage this condition. It turned out, however, that taking calcium supplements is not as safe as it was believed. Women with cerebrovascular diseases such as stroke and white matter lesions are at much higher risk of developing dementia when they regularly take calcium supplements. The risk is 7 times higher among women with a history of stroke who take supplements compared to women with a history of stroke who don’t supplement their diet with calcium. The molecular mechanism behind this phenomenon remains unclear.

Drugs for epilepsy may cause psychotic disorders

People with epilepsy are known to be prone to psychiatric disorders, but it appears that the part of problem is the very drug used to control epileptic seizures. New study revealed that in one out of seven epilepsy patients, the psychiatric disorders can be attributed to the use of this drugs. Women and people with temporal lobe epilepsy are particularly vulnerable to this side effect.

Better education of clinicians needed to avoid misdiagnosis of multiple sclerosis

Due to its rather unspecific manifestations and the lack of reliable biomarkers, multiple sclerosis (MS) can be a challenging condition to diagnose correctly. New study suggests that numerous patients misdiagnosed with other conditions received potentially harmful treatment for a disease they didn’t have. Moreover, the study also shows that in most cases the misdiagnoses were linked to not following the existing diagnostic guidelines and criteria correctly. Better education of clinicians is required to avoid misdiagnosis of MS and recognising patients who were diagnosed incorrectly.



Sanne Kikkert, James Kolasinski, Saad Jbabdi, Irene Tracey, Christian F Beckmann, Heidi Johansen-Berg, Tamar R Makin. Revealing the neural fingerprints of a missing hand. eLife, 2016; 5 DOI: 10.7554/eLife.15292

Svetlana Hakobyan, Katharine Harding, Mohammed Aiyaz, Abdul Hye, Richard Dobson, Alison Baird, Benjamine Liu, Claire Louise Harris, Simon Lovestone, Bryan Paul Morgan. Complement Biomarkers as Predictors of Disease Progression in Alzheimer’s Disease. Journal of Alzheimer&8217;s Disease, 2016; 1 DOI: 10.3233/JAD-160420

Saïda Abounit et al. Tunneling nanotubes spread fibrillar ?-synuclein by intercellular trafficking of lysosomes. The EMBO Journal, 2016 DOI: 10.15252/embj.201593411

Quan Lu, David C. Christiani, Robert O. Wright, Tomas R. Guilarte, Kirstie Stanfield, Li Su, Yongyue Wei, Rory Kirchner, Zhaoxi Wang, Hae-Ryung Park, Peter J. Wagner. In Vitro Effects of Lead on Gene Expression in Neural Stem Cells and Associations between Upregulated Genes and Cognitive Scores in Children. Environmental Health Perspectives, 2016; DOI: 10.1289/EHP265

Joshua B. Black, Andrew F. Adler, Hong-Gang Wang, Anthony M. D’Ippolito, Hunter A. Hutchinson, Timothy E. Reddy, Geoffrey S. Pitt, Kam W. Leong, Charles A. Gersbach. Targeted Epigenetic Remodeling of Endogenous Loci by CRISPR/Cas9-Based Transcriptional Activators Directly Converts Fibroblasts to Neuronal Cells. Cell Stem Cell, 2016; DOI: 10.1016/j.stem.2016.07.001

Alfonso J. Alfini, Lauren R. Weiss, Brooks P. Leitner, Theresa J. Smith, James M. Hagberg, J. Carson Smith. Hippocampal and Cerebral Blood Flow after Exercise Cessation in Master Athletes. Frontiers in Aging Neuroscience, 2016; 8 DOI: 10.3389/fnagi.2016.00184

Mariana Gabi, Kleber Neves, Carolinne Masseron, Pedro F. M. Ribeiro, Lissa Ventura-Antunes, Laila Torres, Bruno Mota, Jon H. Kaas, Suzana Herculano-Houzel. No relative expansion of the number of prefrontal neurons in primate and human evolution. Proceedings of the National Academy of Sciences, 2016; 201610178 DOI: 10.1073/pnas.1610178113

Jürgen Kern, MD, PhD et al. Calcium supplementation and risk of dementia in women with cerebrovascular disease. Neurology, August 2016 DOI: 10.1212/WNL.0000000000003111

Ziyi Chen, Ana Lusicic, Terence J. O’Brien, Dennis Velakoulis, Sophia J. Adams, Patrick Kwan. Psychotic disorders induced by antiepileptic drugs in people with epilepsy. Brain, 2016; aww196 DOI: 10.1093/brain/aww196

Andrew J. Solomon, Dennis N. Bourdette, Anne H. Cross, Angela Applebee, Philip M. Skidd, Diantha B. Howard, Rebecca I. Spain, Michelle H. Cameron, Edward Kim, Michele K. Mass, Vijayshree Yadav, Ruth H. Whitham, Erin E. Longbrake, Robert T. Naismith, Gregory F. Wu, Becky J. Parks, Dean M. Wingerchuk, Brian L. Rabin, Michel Toledano, W. Oliver Tobin, Orhun H. Kantarci, Jonathan L. Carter, B. Mark Keegan, Brian G. Weinshenker. The contemporary spectrum of multiple sclerosis misdiagnosis. Neurology, 2016; 10.1212/WNL.0000000000003152 DOI: 10.1212/WNL.0000000000003152

Image via skeeze / Pixabay.

Does Moderate Alcohol Consumption Improve Brain Function?

It is well documented that excessive consumption of alcohol is linked to various serious health problems. Heavy drinking is a known risk factor for diseases such as cardiovascular problems, some types of cancer, cirrhosis, dementia, depression, pancreatitis and high blood pressure, among others.But what about low-to-moderate alcohol consumption?

A number of studies published in recent years present a view rather different from the traditional negative assumptions. Contrary to popular beliefs, they claim that moderate alcohol intake can be beneficial.

Let&8217;s first define what is heavy and what is moderate drinking. If you are a male and drink at least 15 drinks every week, then you are considered a heavy drinker. If you are female, 8 drinks per week are enough to put you in this category. On the other hand, if you are a male and do not exceed 2 drinks per day you are a moderate alcohol consumer. For a female, the limit is 1 drink per day.

It is important, however, to remember that the above numbers are based on average statistics: some people are more sensitive to the effects of alcohol than others. This sensitivity depends on the level of the enzyme alcohol dehydrogenase in the liver, which metabolizes ethanol and removes it from the body. When the level of this enzyme in an individual is low (as often is the case in many people with Asian background, for example), the effects of low alcohol doses are much more pronounced.

Studies show that moderate alcohol intake can reduce the risk of cardiovascular diseases, dementia, depression, stroke, breast and colon cancer. However, there is always a risk that moderate alcohol consumption can lead to much heavy drinking.

One recently published prospective study examined the influence of moderate alcohol consumption on the development of depression. This study was extensive and included over 5,500 men and women, all of whom had no previous depression or any alcohol-related problems. All participants were moderate drinkers and were followed for a period of seven years. The results clearly show that low and even moderate alcohol consumption reduced the risk of depression development compared to non-drinkers. However, heavy drinkers are known to be in greater danger of developing depression. Another interesting fact demonstrated by this study is that moderate wine consumption has a better protective role in the prevention of depression than any other kind of alcohol beverage.

Another prospective study included over 13,600 people that were followed for a period of ten years. The results show that moderate alcohol intake in females can reduce the risk of depression.

Alzheimer&8217;s disease is one of the serious diseases for which there is no real cure at present time. Because of that, it is important to find risk factors promoting its development, as well as factors which can reduce that risk. Some researchers are focusing on the role of alcohol consumption in the development of Alzheimer&8217;s disease. One of the main features of Alzheimer&8217;s disease is an aggregation of beta-amyloid in the human brain.

A recent Finnish study was examining the connection of aggregation of beta-amyloid in the human brain and alcohol consumption. The results of this study show that the aggregation of beta-amyloid in the human brain is lower among beer drinkers. There was no connection between lower amounts of beta-amyloid in the human brain and consumption of any other types of alcohol.

In another study, over 3,000 people were examined for a period of six years. Some of the participants suffered from milder forms of memory loss. The alcohol intake also varied among the subjects. The results clearly show that moderate alcohol intake had a protective effect on memory for individuals which had no previous memory problems.

The problems with memory can be caused by vascular problems. Since the benefit of moderate alcohol intake on the cardiovascular system is well known, scientists thought that it may work the same way in the prevention of memory problems. They followed a group of nearly 8,000 people and recorded their alcohol consumption and symptoms of memory problems. Their main conclusion was that moderate alcohol consumption can reduce the risk of dementia in people above 55 years of age. There is a large number of studies which were done on this topic and the conclusions were the same: moderate alcohol consumption reduces the risk of Alzheimer&8217;s disease and cognitive impairment.

Recent reports also brought to light the findings that moderate alcohol consumption can influence the size of the hippocampus in elderly population. Compared to abstainers, moderate drinkers have a larger hippocampus and better episodic memory.

So, the scientific data point to the benefits of moderate drinking: it may help to keep a higher level of cognition and prevent age-related deterioration of brain functions. The key is not to go over your limit. Keep your alcohol intake on a moderate level and stay healthy.


Downer, B., Jiang, Y., Zanjani, F., &038; Fardo, D. (2014). Effects of Alcohol Consumption on Cognition and Regional Brain Volumes Among Older Adults American Journal of Alzheimer&8217;s Disease and Other Dementias, 30 (4), 364-374 DOI: 10.1177/1533317514549411

Gea, A., Beunza, J., Estruch, R., Sánchez-Villegas, A., Salas-Salvadó, J., Buil-Cosiales, P., Gómez-Gracia, E., Covas, M., Corella, D., Fiol, M., Arós, F., Lapetra, J., Lamuela-Raventós, R., Wärnberg, J., Pintó, X., Serra-Majem, L., &038; Martínez-González, M. (2013). Alcohol intake, wine consumption and the development of depression: the PREDIMED study BMC Medicine, 11 (1) DOI: 10.1186/1741-7015-11-192

Kok, E., Karppinen, T., Luoto, T., Alafuzoff, I., &038; Karhunen, P. (2016). Beer Drinking Associates with Lower Burden of Amyloid Beta Aggregation in the Brain: Helsinki Sudden Death Series Alcoholism: Clinical and Experimental Research, 40 (7), 1473-1478 DOI: 10.1111/acer.13102

Lang, I., Wallace, R., Huppert, F., &038; Melzer, D. (2007). Moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence Age and Ageing, 36 (3), 256-261 DOI: 10.1093/ageing/afm001

Neafsey, E., &038; Collins, M. (2011). Moderate alcohol consumption and cognitive risk Neuropsychiatric Disease and Treatment DOI: 10.2147/NDT.S23159

Image via Unsplash / Pixabay.

Link Between Diabetes and Alzheimer’s Disease

Rates of Alzheimer&8217;s disease (AD) are rising worldwide, and research on the subject, particularly risk factors and correlation with cognitive impairment and decline are among the most important and applicable. Among those, data suggests that diet seems to be the most important risk factor to target.

For instance, is a very well-known fact that when Japan made the transition from the traditional Japanese diet towards the Western diet, AD rates rose 6% in about 20 years. But diet is also related to certain forms of diabetes, and Type-2 diabetes mellitus (T2DM) is widely recognized as an important risk factor for some forms of dementia. Research about the link between AD and T2DM have concluded that working memory and executive control, for instance, decline in the T2DM compared to healthy people. This decline is lesser in extent than those suffered by AD patients.

An even more important fact is that non-controlled T2DM is strongly related to Mild Cognitive Impairment (MCI) and AD worsening: a study found lower whole-brain volume in participants with both MCI and T2DM compared with participants who had MCI but not T2DM.

Similarly, measured neural activity in their frontal lobe (associated with higher mental functions and reasoning alongside with behaviour), sensory motor cortex (involved in the planning, control, and execution of voluntary movements), and striatum (mediates cognition involving motor function) measured as a function of glucose uptake in those areas, was lower in participants with both MCI and T2DM, than participants with MCI alone. All of this is evidence that T2DM may accelerate and worsen cognition deterioration in patients with AD by affecting glucose metabolism and brain volume.

So, glycemic control is highly encouraged for T2DM and may be beneficial for decreasing the incidence of AD and delaying its progression in diabetic patients.

Yet a third variable linked to both T2DM and AD, is Apolipoprotein E (APOE): among 94 T2DM-patients from the Framingham Heart Study Database, results demonstrated that AD was far more severe in T2DM-patients who were also APOE carriers.

The long-term impact of diabetes on the brain

The process that involves diabetes damaging the brain, leading to AD is well known: it involves pathological mechanisms including cerebral hypoperfusion and glucose hypometabolism. Both of them trigger inflammation and oxidative-nitrosative stress that in turn decrease nitric oxide and enhance amyloid-beta deposition, cerebral amyloid angiopathy, and blood-brain barrier disruption.

All of those changes are long lasting because they involve long-term damage of fatty acids, proteins, DNA, and mitochondria in neurons and glia. This, in turn, perpetuates energy metabolism dysfunction and amyloid-beta generation.

The end result is chronic cerebral hypoperfusion producing synaptic malfunction and neuronal degeneration, leading to both grey and white matter atrophy and AD. Other studies also observed increased glucose intolerance accompanied by the formation of advanced glycation end-products, and activation of the receptor for these end-products. These changes are thought to contribute to the processing of amyloid-beta precursor proteins and decreased amyloid-beta degradation.

One gene to cure them all?

On the other hand, one mechanism by which AD could influence and worsen diabetes was less known until recently. Physiological and molecular analyses demonstrated that centrally expressed human BACE-1 induced systemic glucose intolerance alongside a fatty liver phenotype, impaired hepatic glycogen storage, brain glucose hypometabolism, altered neuronal insulin-related signalling and increased forebrain and plasma lipid accumulation (i.e. triacylglycerols and phospholipids, mainly) in mice.

Even if this study is very recent and lacks some important details, it could demonstrate that there is one gene that regulates both glucose metabolism and amyloid production. This means that by targeting only one gene both diseases could be prevented or even stopped from progressing once any or both of them were diagnosed.

Dealing with AD and diabetes

Even if T2DM is a very important risk factor for AD, diet and a healthy lifestyle are also important to counter progression and onset of AD. Most of the recommendations that follow would decrease the risks of both T2DM and AD, if followed correctly and permanently over the long run.

Current research concerning diet for patients with high risk of AD draws no definitive dietary recommendations. However, high consumption of fats from fish, vegetable oils, non-starchy vegetables, low glycemic index fruits and a diet low in foods with added sugars and moderate (red) wine intake should be encouraged and seem to be one of the best patterns of consumption to prevent both diseases. This was the conclusion of a dietary research of 35 nutrients associated with cognitive function and AD.

Nutrient combinations were assessed using the Harvard/Willet Food Frequency Questionnaire. The identified most &8216;AD-protective&8217; nutrient combination was mentioned above. And it came as no surprise as this combination is regarded as Mediterranean Diet and proved to be useful for preventing cardiovascular diseases and cognitive deterioration in almost every study performed on the subject.

However, diet can only slow down the onset of both T2DM and AD, no improvement of the already existing damage have been achieved through diet or any other mean. Controlling blood sugar is a great start for those who suffer AD and T2DM, but it can’t reverse the existing damage to the brain from AD or the damage of the peripheral tissues from T2DM.

Both for diabetes and Alzheimer’s disease, modern gene therapy shows promise and could achieve human genome manipulation in a decade or two leading to the cure of those conditions. Diabetes could be one of the first to be treated because it is a high-prevalence disease (about 6-8% of the entire world population have it, and increasing) and current research shows that a limited amount of genes are related to it.

Alzheimer’s disease could be a different story, as this is a multifactorial disease. Although, if involvement of BACE-1 is confirmed, both diseases could be treated by targeting one single gene. Curing T2DM and AD would be a great achievement for humanity, as both of them individually are among the most prevalent, disabling and costly chronic diseases of the 21st century.


Berti, V., Murray, J., Davies, M., Spector, N., Tsui, W., Li, Y., Williams, S., Pirraglia, E., Vallabhajosula, S., McHugh, P., Pupi, A., de Leon, M., &038; Mosconi, L. (2014). Nutrient patterns and brain biomarkers of Alzheimer’s disease in cognitively normal individuals The journal of nutrition, health &038; aging, 19 (4), 413-423 DOI: 10.1007/s12603-014-0534-0

Daulatzai, M. (2016). Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer&8217;s disease Journal of Neuroscience Research DOI: 10.1002/jnr.23777

Grant, W. (2016). Using Multicountry Ecological and Observational Studies to Determine Dietary Risk Factors for Alzheimer&8217;s Disease Journal of the American College of Nutrition, 35 (5), 476-489 DOI: 10.1080/07315724.2016.1161566

Guo, C., Zhang, S., Li, J., Ding, C., Yang, Z., Chai, R., Wang, X., &038; Wang, Z. (2016). Chronic hyperglycemia induced via the heterozygous knockout of Pdx1 worsens neuropathological lesion in an Alzheimer mouse model Scientific Reports, 6 DOI: 10.1038/srep29396

Li, W., Risacher, S., Huang, E., Saykin, A., &038; , . (2016). Type 2 diabetes mellitus is associated with brain atrophy and hypometabolism in the ADNI cohort Neurology DOI: 10.1212/WNL.0000000000002950

Matthews DC, Davies M, Murray J, Williams S, Tsui WH, Li Y, Andrews RD, Lukic A, McHugh P, Vallabhajosula S, de Leon MJ, &038; Mosconi L (2014). Physical Activity, Mediterranean Diet and Biomarkers-Assessed Risk of Alzheimer&8217;s: A Multi-Modality Brain Imaging Study. Advances in molecular imaging, 4 (4), 43-57 PMID: 25599008

Perrone L, &038; Grant WB (2015). Observational and ecological studies of dietary advanced glycation end products in national diets and Alzheimer&8217;s disease incidence and prevalence. Journal of Alzheimer&8217;s disease : JAD, 45 (3), 965-79 PMID: 25633677

Pluci?ska, K., Dekeryte, R., Koss, D., Shearer, K., Mody, N., Whitfield, P., Doherty, M., Mingarelli, M., Welch, A., Riedel, G., Delibegovic, M., &038; Platt, B. (2016). Neuronal human BACE1 knockin induces systemic diabetes in mice Diabetologia, 59 (7), 1513-1523 DOI: 10.1007/s00125-016-3960-1

Redondo, M., Beltrán-Brotóns, J., Reales, J., &038; Ballesteros, S. (2016). Executive functions in patients with Alzheimer&8217;s disease, type 2 diabetes mellitus patients and cognitively healthy older adults Experimental Gerontology, 83, 47-55 DOI: 10.1016/j.exger.2016.07.013

Solfrizzi, V., Panza, F., Frisardi, V., Seripa, D., Logroscino, G., Imbimbo, B., &038; Pilotto, A. (2014). Diet and Alzheimer’s disease risk factors or prevention: the current evidence Expert Review of Neurotherapeutics, 11 (5), 677-708 DOI: 10.1586/ern.11.56

Solfrizzi, V., Panza, F., Frisardi, V., Seripa, D., Logroscino, G., Imbimbo, B., &038; Pilotto, A. (2014). Diet and Alzheimer’s disease risk factors or prevention: the current evidence Expert Review of Neurotherapeutics, 11 (5), 677-708 DOI: 10.1586/ern.11.56

Image via jaytaix / Pixabay.

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