Why You Might Be At Risk For Alzheimer's

In recent studies, it has been discovered that if your father was diagnosed with Alzheimer's, it's possible that he can pass it down to you. This is due to the greater spread of tau proteins in their brains, when they develop Alzheimer's. Up to now, it's always been believed, that the risk of Alzheimer's being passed down, was based on the mothers, we learn now, that this isn't the case. Women, however are still more at risk than men are of developing Alzheimer's, because they tend to have a heavier build-up of tau in their brains, making them more susceptible. According to HealthDay, it's also likely that more women develop Alzheimer's than men because, on average, they tend to live longer.

When reading this article, I found it interesting that Fathers are able to pass Alzheimer's disease down, because, I was only aware that mothers could pass it down. Even on TV shows, we only ever see mothers developing the disease. I feel like, now knowing it's possible for our fathers to pass the disease down, it shines a new light on this devastating disease. 

42 previously unknown genes discovered for Alzheimer's disease

In the biggest study of Alzheimer's disease genetic risk to date, researchers discovered an additional 42 genes linked to the disease's development. The study has been going on for 30 years now, as said by co-author Julie Williams, center director at the UK Dementia Research Institute at Cardiff University. She also added that smoking, exercise, and diet are all factors that impact the development of Alzheimer's disease, and taking steps to address them now is a good strategy to reduce our risk. However, Williams also said "60-80% of disease risk is based on our genetics and therefore we must continue to seek out the biological causes and develop much-needed treatments for the millions of people affected worldwide." Apart from the well-known APOE e4 gene and the production of amyloid-beta and tau, two signature proteins that pile up in the brain with disastrous consequences as Alzheimer's progress, the previously unknown genes suggest new pathways for disease progression. According to the study, a number of the newly discovered genes are involved in highly complex interactions between proteins in the body that determine how inflammation and the immune system might harm brain cells. This discovery will provide scientists with new targets for treatments, drugs, and lifestyle modifications that could help people avoid developing this fatal brain disease. The genomes of 111,326 people with clinically diagnosed Alzheimer's disease were compared to genes from 677,663 cognitively healthy people in a global study. Data was taken from clinics from over 15 European Union countries, as well as the United States and more. The study found 75 genes associated with an increased risk of Alzheimer's disease, 33 of which were previously unknown. It also backed up years of research into the roles of amyloid-beta and tau in Alzheimer's disease. Many of the 42 identified genes linked to Alzheimer's disease clustered into numerous suggested but unverified disease development pathways. One of the main pathways that are being suggested is the immune system, which is designed to defend us from germs. LUBAC, an immunological regulator required by the body to activate genes and prevent cell death, was linked to a number of genes. Microglia, immune cells in the brain entrusted with clearing away damaged neurons also play a vital role in persons with Alzheimer's disease, according to the study. According to the study, genes linked to inflammation are another important pathway. Inflammation is a defense mechanism used by the body to eliminate germs, but it also helps to remove damaged cells. With more additional studies, it was found that Alzheimer's could be a multifactorial disease, made up of different types of pathogens. Another important finding of the study was that neurodegenerative diseases including Parkinson's, frontotemporal dementia, Lewy body disease, and amyotrophic lateral sclerosis may share the same genetic origin, implying that there is a continuum between them. The authors of the study devised a new scoring method to estimate the risk of Alzheimer's disease as a result of obtaining a more thorough picture of hereditary risk. This would change the future, as scientist will be able to locate, Alzheimers in a patients, and find ways to stop, or even narrow the disease down before it taking over the body.

LaMotte, Sandee. “42 Previously Unknown Genes Discovered for Alzheimer's Disease.” CNN, Cable News Network, 6 Apr. 2022, https://www.cnn.com/2022/04/05/health/new-alzheimers-genes-wellness/index.html.

“Study on Genetic Risk for Alzheimer's Discovers 42 Previously-Unknown Genes Linked to the Disease.” The Indian Express, 6 Apr. 2022, https://indianexpress.com/article/lifestyle/health/study-genetic-risk-alzheimers-42-unknown-genes-linked-disease-7855956/.

Native American DNA can reduce risk of Alzheimer's Disease

 

Our genes influence illnesses such as cancer, heart disease, depression, and Alzheimer's. A recent study involved two researchers working to find out which genes affect people’s risk for certain diseases. During their research, they saw that there is a genetic region that is protective against Alzheimer’s disease. They used the method of admixture mapping to find the genetic causes of the disease. Specifically, they applied this method to a population of Caribbean Hispanic people who have a mix of Native American, African, and European ancestry. In doing so, these researchers found that individuals with Native American ancestry were less prone to developing Alzheimer’s disease. That said, simply identifying as or looking Native American does not protect against the disease. One must have Native American ancestry at a specific point in the genome to be less susceptible to the disease.

While this research may not lead to the cure for Alzheimer’s, this research is incredibly helpful to understanding the disease, its causes, treatments, and why certain ethnicities are more or less prone to this debilitating condition.




Article Link:

https://www.psypost.org/2021/07/mixed-ancestry-genetic-research-shows-a-bit-of-native-american-dna-could-reduce-risk-of-alzheimers-disease-61554




Related Link:

https://moneyweek.com/investments/stocks-and-shares/biotech-stocks/603570/investing-in-alzheimers-drugs

A Molecule Eliminates Clumps of Amyloid Proteins Found in Alzheimer's Disease.

 

This article highlights researchers, from the University of Tokyo, who injected mice, with Alzheimer's Disease, with a small, light-activated molecule. This molecule eliminates clumps of amyloid proteins, found in Alzheimer's Disease. Alzheimer's, ultimately, destroys neurons and their connections in parts of the brain involved with memory and later affects the cerebral cortex, which is responsible for language, behavior and reasoning. This article talks more about what Alzheimer's Disease does to the brain.  Researchers, then, shined a light, using a probe, into their brains, for 30 minutes, each day, for one week. The chemical analysis of the brain tissue showed that there was a significant reduction of the amyloid protein. Human brains have also been donated to support this research in the hopes of using it on live patients, one day. 

Thirteen New Alzheimer's Genes Identified: What This Could Mean.

 

    In an article posted on neurosciencenews.com titled "Thirteen New Alzheimer’s Genes Identified", a whole genome sequencing study is outlined to have revealed thirteen new genes linked to Alzheimer's Disease, as well as a novel link between synaptic function and Alzheimer's. Led by Dr. Rudolph Tanzi, PhD, vice chair of Neurology and director of the hospital’s Genetics and Aging Research Unit, this study is the first of its kind to utilize whole genome sequencing in the context of Alzheimer's research, as the genome wide association study (GWAS) was previously used as the predominant mode of identifying AD genes. The cons of the GWAS are established in the article, stating "A standard GWAS misses the rare gene variants (those occurring in less than 1% of the population), a problem solved by the WGS, which scans every bit of DNA in a genome (Neuroscience News, 2021). As expressed, the WGS process of the study was comprehensive, with the whole genomes of 2,247 individuals from 605 families (with documented AD diagnoses), and 1,669 unrelated individuals being analyzed.

            The thirteen identified novel genes are associated with synaptic function, neurodevelopment/neurogenesis, and neuroplasticity. This newly established understanding of the involvement of synaptic function and neuroplasticity with AD may suggest that genetic predisposition and/or epigenetic markers pertaining to abnormal synaptic function are far more important in the development of AD than previously thought. With this in mind, new research which specifically explores synaptic function/dysfunction and neuroplasticity in AD patients of varying stages would shed immense light into how these genes are manifested as functional phenotypic expressions. This research may also confirm the Amyloid Hypothesis and its connection with synaptic dysfunction (The accumulation of oligomerized, self-aggregated amyloid-beta is the primary cause of synaptic dysfunction, the buildup of senile plaques, and subsequent neurodegeneration), though the Tau Hypothesis may also be confirmed with the same logic, as Tau neurofibrillary tangles are also a demonstrable cause of synaptic dysfunction. Another unexplored question pertaining to the research is the following; Did these genes express prior to, or only after the development of AD? If these genes are expressed prior to the development of AD, then development of the disease may be highly predicated on the expression of such genes. Conclusively, the use of WGS in AD research to identify these thirteen genes is groundbreaking, and new drugs which target synaptic function and potentially initiate neurogenesis may prove to be hopeful developments in the treatment of Alzheimer's. 

References & Information:

Article: https://neurosciencenews.com/alzheimers-novel-genes-18168/

Alzheimer's Disease: https://www.alz.org/alzheimers-dementia/what-is-alzheimers#:~:text=Alzheimer's%20is%20a%20progressive%20disease,and%20respond%20to%20their%20environment.

Alzheimers gene linked to Corona virus

The APOE4 gene variant has been known for creating a greater risk for a person to develop Alzheimer's disease. This same gene variant is also linked to the novel Covid-19. Based on a study published by "The journals of Gerontology", it has been determined than an individual who carries two copies of the gene variant are twice as likely to develop a severe case of the covid-19. The APOE4 gene variant also affects cholesterol transport and inflammation. 383,000 individuals of European background were included in the study and more than 9,000 carried 2 copies of this gene variant. The list of people with two copies of the gene variant and those that suffered from covid-19 were cross referenced. The result showed that the APOE4 homozygous genotype was linked to a doubled risk of his severe disease as opposed to those individuals who had 2 copies of another gene variant known as E3

Source 1:    https://www.the-scientist.com/news-opinion/alzheimers-gene-linked-to-higher-risk-of-severe-covid-19-67570

Source 2: https://www.alz.org/alzheimers-dementia/coronavirus-covid-19

CHRFAM7A Gene Explains Why Alzheimer’s Drugs Fail in Humans

Alzheimer’s disease is an irreversible and progressive brain disorder that destroys memory and thinking. This disease eventually effects a person’s ability to complete simple, everyday tasks. Alzheimer’s is currently ranked as the sixth leading cause of death in the United States. Although scientists do not understand what causes Alzheimer’s disease, some believe a genetic mutation may be the cause. 

Photo credit: https://www.drugwatch.com/health/alzheimers-disease/

According to Medical News Today, Dr. Kinga Szigeti, director of the Alzheimer’s Disease and Memory Disorders Center at the University of Buffalo, found a gene that helped explain why Alzheimer’s drugs appear useful in animals but not in humans. The gene, CHRFAM7A is a fusion gene for alpha-7 nicotinic acetylcholine receptor- a neurotransmitter receptor, acetylcholine, and kinase. Acetylcholine has been linked with the development of Alzheimer’s and plays a crucial role in memory and learning. In Dr. Szigeti’s recent study, she and her team focused on how this CHRFAM7A gene relates to drug effectiveness in humans. 

The study concludes CHRFAM7A is present in two variations, a functional one and one that is not translated into a protein. Even though this gene is specific to humans, only 75% actually have it. Further, three out of four of Alzheimer’s drugs that are available target all of the acetylcholine receptors. Ironically, drugs that specifically target the alpha-7-acetylcholine receptor, have failed in humans. Essentially, an individual's genotype determines what drugs demonstrate to be effective.

"People who don't have the [CHRFAM7A] gene respond better to the drugs available now," Dr. Szigeti reports, "our work confirms that Alpha 7 is a very important target for treating Alzheimer's but the right model — a human model — has to be used when testing new drugs.” In other words, more personalized drugs are necessary for treatment because of the differentiation in humans. A drug may work for 75% of people with Alzheimers, but fail in the remaining 25% or vice versa. 

This article is very interesting but also may raise a lot of concerns that I do not think people are ready to talk about. A few questions that come to my mind would be (a) When is it acceptable to test drugs on people? (b) Would drugs have clinical trials and patients willingly test different methods? (c) How does this affect the pharmaceutical industry and will be personalized drugs become available? Other than human testing, I think this CHRFAM7A gene and its explanation for drugs presents a lot of opportunities for the future of genetics and pharmaceuticals. 

Sleep Deprevation Accelerates Alzheimer's

At the Washington University School of Medicine, researchers discovered that sleepdeprivation causes the levels of tau to increase, and tau is a key protein for Alzheimer’s. The researchers have been doing studies on mice to observe how lack of sleep can increase the protein of tau in the brain. Lack of sleep may be a factor on how fast the disease of Alzheimer’s spreads to the brain because the lack of sleep causes tau proteins to become damage and spread over time. Researchers found out that tau is higher in elderly people who do not get enough sleep and they wanted to find out if lack of sleep could be a major contributor to Alzheimer’s. As the researchers examined tau levels in mice, they found out by disrupting mice’s sleep during the day time, because mice sleep during the day, that tau levels almost doubled in the mice’s brain. The researchers then decided to test tau levels on humans, by testing their tau levels after getting a good night’s rest and then after getting no sleep, and they discovered that the tau levels increased about fifty percent. Tau tangles together in parts of the brain responsible for memory which can cause people to struggle to think clearly and lead to Alzheimer’s disease. 

I found this article to be very interesting because I know there is no cure to Alzheimer’s disease, but researchers are now discovering that lack of sleep can be a contributor to the increase of how fast Alzheimer’s develops in the brain. Researchers are always saying how good sleep is for having a healthy life style, and now it is important to get enough sleep at night to prevent the increase of tau proteins from building up in the brain. Although, it does not say how much faster Alzheimer’s will develop in a person from lack of sleep, but it is always important to try to get enough sleep at night.

The Gene's Role in Opioid Addiction

     A recent study published in the journal Biological Psychiatry showed there is a possible link between the human gene and addiction to opioids. Researchers analyzed over 5,000 Americans that had been exposed to opioids. They analyzed the differences between those who developed a dependence to the pain killers and those who did not exhibit any signs of dependence. As an opioid epidemic is currently affecting a large portion of our population, it is imperative that we find a way to combat it. Researchers found a genetic abnormality on a chromosome. Located near gene RGMA, it has been associated with opioid dependence in European and also in African-Americans. As a testament to the quality of the research, members of the same team found other genetic variants that were closely related to opioid dependence in the past as well. They also discovered that through analyzing human gene expression in the brain that there was a direct correlation between the RGMA gene and a handful of other genes which have been linked to disorders like autism, Alzheimer’s and schizophrenia.

     This research is vital more than ever in society today. Millions of Americans suffer from opioid dependence across the country. With consequences as severe as death, this problem needs a solution and fast. And although this is merely a potential solution to the epidemic, it is still a step in the right direction. Also, they found correlations with the other disorders listed above. This research could serve as a stepping stone toward furthering our knowledge and possibly curing them in the long run. 

Article Link: https://www.cnn.com/2018/02/22/health/genome-genetic-opioid-addiction-study/index.html

Study Link: http://www.biologicalpsychiatryjournal.com/article/S0006-3223(18)30028-3/fulltext

Brain-aging gene discovered

A new discovery has been found in adults around age 65 that greatly affects their aging of their brain. Columbia University Medical Center found that the gene TMEM106B has different variants that causes this abnormal aging in older adults. After studying data from various autopsied brain samples, researchers came up with a measure called differential aging. Differential aging is the difference between an individuals apparent age (biological) and their true age (chronological). This gene TMEM106B begins to take effect once people reach the age of 65 but researchers found a second variant inside the proganulin gene that affects brain aging as well. These two genes are found on separate chromosomes but are in the same signaling pathway.

It seems like if you have these genetic variants then brain aging is accelerated and causes you to be more vulnerable to brain diseases like Alzheimer's. These discoveries could help researchers to look into potential new targets for preventing and treating certain brain aging diseases.

Link to article

More Info

A Cup of Tea can Keep the Dementia Away

https://www.sciencedaily.com/releases/2017/03/170316093412.htm

http://www.medicalnewstoday.com/articles/316619.php

        It has been recently discovered that consuming a cup of tea daily will decrease the risk of cognitive decline in the elder years. Research led by Assistant Professor Feng Lei at National University of Singapore's Yong Loo Lin School of Medicine, reported a 50% decrease in normal individuals. This was pretty low compared to individuals who carry the APOE e4 gene whose percent decrease went up by 85%. APOE e4 is a gene that puts people genetically at a higher risk for developing Alzheimer's disease.
       The benefits of tea consumption come from the tea leaves themselves. There are bioactive compounds in the leaves that demonstrate anti-inflammatory and antioxidant advantages. Some other compounds help protect the brain from vascular damage and from degeneration, thus preventing diseases like Dementia.  This is new and exciting news in the medical community and further research is being done to help support these findings.

F.D.A. Will Allow 23andMe to Sell Genetic Tests for Disease Risk to Consumers

      A company named 2andMe based in Mountain View, California has long sought the green light to sell consumers genetic tests. The Food and Drug Administration is allowing the company 23andMe to sell genetic test kits to consumers, this will allow them to test for the likelihood that they will inherit genetic diseases such  as Alzheimer's. Currently the companies test only include ten diseases including Parkinson , Celiac disease, Alzheimer's, Gaucher disease type 1, etc.  This landmark decision for the FDA is expected to allow more companies to release tests directly to the consumer. The health kit sold by 23andMe is retailed for $199.00 and is a simple process.

   

    After a customer purchases the kit they then spit into a tube and mail it o the 23andMe headquarters. The companies lab will extract DNA from the saliva and test it against genetic markers for certain diseases. The customer can then log into their account and see the report and its interpretation. Although i believe this is a big step in allowing the public to readily know if they are carrying a disease, i also find man drawbacks. Most who have a family history of illness may want to know right away if they too inherited the disease and with the new technology can know in a matter of days without properly preparing themselves mentally for the news. Once you have received the results there is no unknowing and that could lead to depression. Also the tests could confuse customers as the results do not indicate you have the disease but that you have a higher likelihood.

https://www.nytimes.com/2017/04/06/health/fda-genetic-tests-23andme.html?_r=0

https://techcrunch.com/2017/04/06/23andme-is-finally-allowed-to-tell-you-if-you-have-the-genes-for-parkinsons/

https://www.23andme.com

Would you like to know if you would develop Alzheimer's?

No one anticipates developing a disease throughout their life but too many of us have experienced or have seen family with the difficulties of an illness. What if there was the possibility to predict what age someone would develop Alzheimer’s disease? Futurism magazine defines the disease as a “progressive deterioration of brain function”, over 5.5 million people are diagnosed in the US, as well as 200,000 suffer from early-onset Alzheimer’s.A genetic test that can calculate age-specific risk of Alzheimer’s development has been created by researchers at the University of California San Diego School of Medicine and University of California San Francisco. The method consists of searching for mutations in genes found in DNA, there are 31 markers, separately the genes would not lead to any abnormal effects, although when established together Alzheimer’s can be predicted to occur in someone’s future. APOE (Apolipoprotein E), the one gene stands out among the rest because with the mutation there is a 15% increase of chance of getting the disease.

The genetic research and testing has opened a new opportunity for the medical field. Pre-testing will lead to using medication for prevention and control. Being able to help someone prepare for their future, but with benefits there are always concerns. Such as, job discrimination if one day the human gnome is required for job applications will someone hesitate to hire someone if they know that the person has a higher chance of developing Alzheimer's disease.

Overall, this research has led to amazing insight into the development of Alzheimer's disease and will continue to flourish as more people donate their DNA. I think this research will be beneficial for patients to have a piece of mind knowing they are doing all in preparation for themselves and their loved ones. For example, if you know that you are going to developed Alzheimer's, if you wish you can stare medication for prevention can be administered, prepare your family when when you may no longer be able to communicate all you would like, spend time doing things that you love and just enjoy life. Knowing that you have something does not always have to be bad news, it allows for appreciation all the little things in life.

https://futurism.com/a-new-genetic-test-predicts-if-and-when-youll-develop-alzheimers/

http://www.telegraph.co.uk/science/2017/03/21/genetic-test-can-tell-age-person-likely-develop-alzheimers/

We cant get rid of Alzheimers yet, but we can keep trying.

Alzheimer's is probably one of the worst diseases anyone can deal with. Although we have yet to find a treatment for Alzheimer's, we can keep trying until we find something. Solanezumab was an experimental Alzheimers drug that promised to slow down the deterioration of thinking and memory, which failed in a large Eli Lilly clinical trial. This was very upsetting to those that were hoping to be treated. The drug was prescribed to those that had mild dementia, the drug was supposed to detect it early on and try to slow down the symptoms. People that develop Alzheimer's sometimes do not show any symptoms. Testing a drug on people that have developed a disease before showing symptoms is challenging and costly.


Solanezumab has also failed in two big clinical trials involving patients with mild or moderate Alzheimers. When Lily reported that the results of those trials , it showed that the drug did have an effect in some patients with mild symptoms. So then they started another trial with 2, 100 patients with mild dementia due to Alzheimer's.

Dr. Eric Reiman, executive director of the Banner Alzheimers Institute raised questions about the drug, he wondered whether Lilly's dose was high enough,whether the researchers were attacking the right form of amyloid, and whether they were treating the patients too late in the disease process. I agree with Dr.Reiman on this, in order for us to attack a disease such as Alzheimer's, we must do research from every angle possible. The treatment for Alzheimer's is probably very close by, but we are just looking in the wrong places. They can start off by fully understanding Alzheimer's from top to bottom, and one of the main causes which are amyloid buildup, which is the buildup of proteins in the brain. We can work on a drug that tries to deteriorate amyloid buildup as it begins to develop in the brain.

Discovering Unknown Gene Mutations in Iceland's DNA

Sequencing genomes is incredibly helpful in adding to the understanding of different species and populations. Having data for sequenced genomes also gives a lot of information for people that study gene mutation and disease. Scientists in Iceland sequenced the complete genomes of 2,636 people from Iceland which is the biggest population sequenced out of every country in the world (in 2015). From this information they were able to also deduce information of the genomes of  more than a hundred thousand other Icelanders, adding to the extensiveness of this feat.

http://travel.nationalgeographic.com/travel/countries/iceland-guide/

This genetic information helped scientists discover how different mutations that were unknown before affect certain diseases. Not all diseases are caused by a mutation on a single gene, mutations of many genes can cause certain disease or the likelihood of someone getting that disease. There are so many different combinations of mutations yet to be discovered, but having a big population size with available genetic information can lead to more because scientists can find things in common with people from the same population. Scientists found that eight people from Iceland with the same mutation on a MYL4 gene all had a diseases that causes irregular heartbeat in common. Having a big sample size to compare data to is very helpful in science, and can help lead the studies of how mutations affect many diseases, progressing. 

http://www.nytimes.com/2015/03/26/science/in-icelands-dna-clues-to-what-genes-may-cause-disease.html?_r=0

3-D Imaging of DNA Migration

At the Lawrence Berkeley National Laboratory, scientists have been able to document the movement and reorganization of genetic material that takes place within a cell through 3-D visualizations. In the image below, researchers developed a 3-D reconstruction of mouse olfactory cells through X-ray imaging tools. The importance of this discovery allows for easier understanding of patterning and reorganization of chromatin within in the cell's nucleus. By understanding how the chromatin is organized within the nucleus, it helps to determine its relation the the cell's specialization in terms of activated or silenced genes.

The process of the 3-D visualization is performed through a powerful X-ray microscope at Berkeley Lab's Advanced Light Source (ALS). Researchers capture images of the cells of interest at different maturity stages as the cell becomes more specialized for its specific function. This process, known as "differentiation", uses different angles of 2-D images to calculate the 3-D reconstruction of the chromatin formation. 

The benefits of the 3-D visualization of the chromatin was not having to chemically treat the cell in order to observe the change in the nucleus. Because chromatin is very sensitive, chemical stains had to be used to indirectly image the cell, assuming the stain was evenly distributed. According to Carolyn Larabell, a faculty scientist at Berkeley Lab, originally hypothesized that chromatin exist as a series of disconnected islands. However, through the 3-D visualization, it was determined that chromatin was all connected and packed within the nucleus. Larabell hopes that new insight into gene expression can be made, especially with their current study of mice olfactory genes.

Through using the mouse olfactory genes as a model for studying, researchers hope to target how the gene expression works within Alzheimer's disease. The disease itself attacks the brain's nerve cells in which can cause a loss in senses such as smell. By using the 3-D imaging technique, scientists can understand the connection of the gene expression to the olfactory nerve cells. By using this study as a precursor, scientists can hopefully use this technique to determine cures for other diseases that attack nerves cells. This study is very important in medicine and cell research because it allows scientists how diseases and disorders are related to gene expression. By targeting which expressed gene causes a disease, drugs can be created that can silence the gene expression, thus leading to a very large breakthrough in medicine. 

Elderly with Alzheimer’s Pathology Found with Superior Memory

Scientists have been studying elderly patients over 90 years old who have superior memory abilities compared to their peers. After their death, it was discovered that some of them had widespread plaque and tangles in their brain, which are correlated with having Alzheimer; Despite the Alzheimer pathology present in their brain, they never showed signs of degenerating memory throughout their entire life.

This new revelation has baffled scientists whom believe that this means there are some factors that are protecting these individuals from the plaque and tangles in their brain—something that makes them “immune to the toxic effects of plaques and tangles.” Their goal: To figure out exactly what these factors are and possibly help stop the further decline of neurons and memory for elderly affected by the Alzheimer’s pathology. Changiz Guela, the Northwestern Medicine lead investigator is planning on looking “at genetic, dietary and environmental influences that could confer protection for neurons against Alzheimer’s pathology.

This new discovery can lead to promising therapies and treatment in the future. It has the potential to save millions off lives and families. 

Resources:

1. Northwestern University. "elderly discovered with superior memory and Alzheimer's Pathology." ScienceDaily. ScienceDaily, 16 Novemvber 2016. <www.sciencedaily.com/releases/2016/11/161116132813.htm>.

2. https://www.sciencedaily.com/releases/2016/11/161116132813.htm