New Noninvasive Alzheimer's Treatment

Recent studies conducted on mice, engineered to have Alzheimer's have revealed that light therapy greatly reduces the effects of the disease on the brain. Alzheimer's is an irreversible genetic condition that affects brain function (cognition and memory), and becomes worse over time. The brain becomes congested with beta-amyloid plaque, gamma oscillations become impaired, and begins to form abnormal tau proteins that form tangles in the brain.

Tests conducted at MIT treated diseased mice with light therapy, inducing gamma oscillations at 40 hertz for one hour, beta-amyloid levels dropped by 50%, the only drawback being that beta-amyloids fully recovered to previous levels within 24 hours of treatment. The light therapy also removes plaque and mutated tau proteins. This gamma oscillation also improves the brains overall ability to get rid of mutated or faulty proteins.

Beta-amyloid plaques

Overall I believe this finding is quite fascinating, and could possibly be a big breakthrough in science and the medical field. It is clearly stated that this study has only been done on mice, but everyone including myself has hopes the effect of light therapy will translate to human beings.

Image taken from http://cdn1.medicalnewstoday.com/content/images/articles/314/314627/beta-amyloid-plaques-between-nerve-cells.jpg

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

Alzheimer Pathology Found in Elderly with Superior Memory

A recent study done by Northwestern Medicine has revealed new vital information on Alzheimer's. The study was done on eight individuals, 90 and older who showed superior memory. Three out of the eight individual's brains qualified as having Alzheimer's plaque and tangles present even though they still had superior memory. When there is too much plaque and tangles in the brain, neurons start to die as a result. This means that even though the Alzheimer's was present in these individuals, something in their body is protecting their brains neurons from the toxic effects of the Alzheimer plaque. If scientists are able to determine what is protecting the neurons, it could lead to new medications for Alzheimer patients.

Certain parts of the brain were looked at. One of those parts was the hippocampus, which was looked at and examined, revealing that the nerves cell in the individual with superior memory were all intact. Than patients brains that did have Alzheimer's and displayed the effects of were looked at, revealing quite the opposite. The nerve cells this time showed a significant amount of dead cells. The lead investigator in this study was Changiz Geula which stated, "'These findings clearly demonstrate the brains of some elderly are immune to the toxic effects of plaques and tangles'"(sciencedaily). A new discovery like this brings hope and may even be the leading point need that points us the right direction.

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

The Genomic Key to Memory

Have you ever thought that your short-term memory was just really bad? Forgetting the name of someone you just met or where you put your keys are common slips in memory that haunt most of us at some point in our lives. For certain individuals these issues will continue to progress with age and lead to signs of detrimental conditions such as Alzheimer's disease. A new study led by Prof. Ian Deary of the University of Edinburgh in the UK identifies specific genes that are linked to poorer memory in life. This was the first international study that found a link between common genetic variants and the ability to recall lists of words and stories.

The study used data from five studies conducted at the University of Edinburgh: the Lothian Birth Cohort 1921 and 1936. Altogether these made up the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium, which analyzed data from 30,000 individuals over the age of 45. The participants, all free of dementia, underwent memory tests that involved recalling words and stories after an assigned time period. It was found that individuals with certain genetic variants had signs of early Alzheimer’s in their brain tissue. The researchers analyzed the results with personal genome data to determine genetic variants and changes that were inked to lower memory.The results show that individuals with lower overall scores had variants near a gene called Apolipoprotein E and other gene involved with immune responses. It should be noted that previous research indicated that some forms of Apolipoprotein E are linked with increased risk of dementia, including Alzheimer's. The researchers also checked 725 postmortem brain tissue samples and determined that individuals with the genetic variants that related to poorer test scores were more likely to have signs of early Alzheimer's disease.

The genetic variants associated with memory performance also predicted altered levels of expression of certain genes in the hippocampus, a key region of the brain for the consolidation of information. This really is an interesting study for me because I do feel like I have really bad memory, and I’m young. I don’t personally have any relatives that suffer from diseases such as Alzheimer’s but the fact that the genes associated with it can be identified can lead to revolutions in the medical aspect. This can help lead the path to new preventative medicines. The data from this study from the memory test can be used in future studies as well.

Two common genetic variants connected to memory performance

            The researchers and scientists from Boston University School of Medicine “have discovered to common genetic variants that are believed to be associated with memory performance.” This is a giant step forward since it can help adults with dementia retain their memory for longer, and be independence for a bit longer. 

Alzheimers linked to Apolipoprotein E gene

The study was conducted under the data that was gathering through “Charge” which is an acronym for Cohorts for Heart and Aging Research in Genomic Epidemiology. They acquired their data from 30,000 dementia free adults over 45 years old, 11,000 candidates of European decent, along with approximately 1,500 young adults to have a comparison between the adults. They were examined by completing memory test that incorporated recalling memories, and they examine segments of their complete genome to certain points that they scored low on the test. In their studies they discovered that the Apolipoprotein E gene had a direct correlation to the candidates low score when remembering, and was known to be a risk of dementia. Along with a section of the genome involving the immune system also had a correlation to the candidates inability to remember.

This is great discovery since this will improve the understanding of memories, and will help people with Alzheimers retain their memories and remain a functional adult. This also shows that by a large collaboration of the scientific community pooling in their data will make it easier and increase the pace of research.  

Article:http://www.news-medical.net/news/20141125/Researchers-discover-two-common-genetic-variants-associated-with-memory-performance.aspx

2nd Article :http://www.myfoxal.com/story/27481703/researchers-uncover-clues-to-memory-performance-in-international-genetic-study

Gene Expression by Brain Immune Cells

A resent study by the Massachusetts General hospital, using a sequencing method has identified a group of genes used by brain immune cells called microgilia which sense pathogenic organisms toxins and damaged cells that require their response. The study has found that these genes activity appears to be protective in respect to aging. Investigators hope that understand these genes will lead to better understanding their role in neurodegenerative disorders like alzheimers and parkinsons disease.

Joesph El Khoury M.D. of the MGH center for immunology and inflammatory diseases and division of infectious diseases stated “for the first time a set of microglia that can sense their environment have been found" and  "identifying these gene will allow us to specifically target them in diseases of the center nervousness system by developing way or unregulated or down regulate their expression." Depending on the situation they encounter microglia may react in a protective manner or releasing toxic substances substances that directly microbes or infected brain cells. However neurotoxic responses can also damage healthy cells contributing to damage caused by neurodegenerative disorders.  "Establishing the sensome of microglia allows us to clearly understand how they interact with and respond to their environment" with nest steps defining the sensome of microglia and other brain cells identifying how they sensome changes in central nervous system disorders to safely manipulate the sensome pharmacologically.

This article was interesting and details how our understanding of human physiology is not only changing but improving. Information from future studies can provide knowledge for therapies and pharmacological treatment.

http://www.sciencedaily.com/releases/2013/11/131114193432.htm
http://www.sciencedirect.com/science/article/pii/S2211124713002969
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277080/

Researchers Find an Epigenetic Culprit of Memory Decline

In HHMI, Dr. Li-Huei Tsai and her team have recently published a mouse model study suggesting that Alzheimer’s disease has epigenetic origins:  her team's studies conclude that a single overactive enzyme is responsible for disabling the expression of other proteins required for neuron functionality.

The primarily culprit seems to be protein HDAC2, an enzyme which belongs to the histone deacetylase family.  A well-studied form of gene regulation is histone acetylation, wherein histones which are enrapt with DNA strands are acetylated.  Aceytlation of the lysine groups on histone tails neutralizes their positive charges, causing a relaxation in binding of the histones to their nucleosome partners.  As a result, transcription factors have an easier access to genes in acetylated regions.  An overactive histone deacetylase such as HDAC2, which deacetylates regions of DNA-histone complex,can thus dramatically reduce the expression of  related key genes necessary for the functionality of any biological processes, in this case neuron functionality.

The study suggests that inhibition of HDAC2 in mouse models resulted in control and experimental groups performing uniformly better in cognitive tests as opposed to their uninhibited HDAC2 counterparts.  Also, post-mortem autopsies of mouse models known to have degenerative disease states have elevated levels of HDAC2.  However, the scientists noted that although inhibition of HDAC2 restored neuron functionality, the rate of neuron cell death remained higher in mutants than in wild-type.  Dr. Tsai suggests that inhibition of HDAC2 'wakes up' malfunctioning neurons that would otherwise be operational; HDAc2 regulation, however, seems for now to be unlinked to increased neuron cell death.

Histopathologic image of senile plaques seen in the cerebral cortex of a person with Alzheimer's disease of presenile onset. Silver impregnation.