Heart Problems Alter Gene Activity in the Hippocampus

    According to the University Medical Center Gottingen, heart problems cause disturbed gene activity in the brain’s memory center. Using mice models, the researchers found that heart failure leads to specific changes in the hippocampal gene expression. This gene directly affects the hippocampus which is a region in the brain that is linked with learning. The changes reflected caused an increase in cellular stress pathways, which eventually lead to loss of neuronal euchromatin and reduced expression of a hippocampal gene cluster essential for cognition. Researchers still do not fully understand why heart failure affects gene activity in the hippocampus.

Article Links:

https://neurosciencenews.com/heart-hippocampus-genetics-17899/

https://www.embopress.org/doi/full/10.15252/emmm.201911900

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

Scientists Prevent Memory Problems Caused by Sleep Deprivation

The hippocampus of a mouse glows green after the neurons are excited by cAMP trigger receptors.

     On November 18, 2014, scientists from the University of Pennsylvania found that a particular set of cells that are located in the hippocampus part of the brain may be responsible for memory issues after an extended amount of sleep loss.  Being that sleep is the most critical period of memory consolidation it has been pojected that lack of sleep may be linked to an extended amount of memory loss due to lack of sleep and memory consolidation.  Robbert Havekes is the lead author of this study conducted in the associated lab of Ted Abel, the study's senior author and Brush Family Professor of Biology in Penn;s School of Arts and Sciences.  Ultimately, Abel's lab published a study in Nature identifying the pathways of AMP and cAMP play a key role in sleep-loss associated with memory issues.  The reason why excitatory neurons were singled out was because of the importance these pathways have in transmitting signals in the brain, as well as their function rely on cAMP signaling.

     To conduct this experiment, mice were used as the test animal and were injected with a non-pathogenic virus that harbored the gene encoding receptor for the protein octopamine.  Octopamine triggers the cAMP pathway in fruit flies but is not naturally found in the brains of mice. Furthermore, after the hippocampus in mice were injected with the non-pathogenic virus, the team confirmed that the only excitatory hippocampal neurons expressed the receptor and that they could selectively increase cAMP levels in the cells that were injected with the octopamine.  Therefore, Havekes concluded that these data display that memory loss due to sleep deprivation is dependent on misregulated cAMP signaling in the excited neurons of the hippocampus.

     I found this article to be quite enticing because I typically do not obtain much sleep each night due to the urge to get extended amount of work done.  Additionally, those who attend Medical School or graduate programs typically do not obtain much sleep from the countless hours spent studying or doing homework, thus does this mean down the line that the individuals who decided to further their education result in a significant chance of lossing their memory?  A very scary thought!

Main article: http://www.sciencedaily.com/releases/2014/11/141118182458.htm

Better Memory Performance linked to Genetic Variant

     The largest study to date of human memory using genomic data was done by the research team of IU School of Medicine, led by post-doctoral medical student Vijay K. Ramanan. This test included over 14,000 older adults. An analysis of genomic data using memory performance test was used to identify a specific location in the genome that was associated with better memory performance. According to an International research team, the results obtained can lead to finding new treatments for memory impairments (such as Alzheimer Disease).

                                        From: http://newsoffice.mit.edu/2013/discovering-hippocampal-connections

      This test involved chromosomal manipulation. There were higher performance tests of episodic memory that was associated with the DNA on chromosome 2; specifically the gene involved a G instead of the more common A nucleotide (in the gene called FASTKD2). The single genetic variant nucleotide polymorphism of SNP was found to also have a denser gray matter in the brain and a slightly larger hippocampus. These foundings were brought by Resonance Imaging Scans.

      This is a fantastic stepping stone for research on genetic variants. More research obviously needs to be done to determine whether the drug targeting the FASTKD2 gene can be used to protect against memory loss. But if these findings are verified, Alzheimer Disease can finally have a treatment associated with it.  

Article from: http://www.medicalnewstoday.com/releases/285378.php
Related article: http://www.ncbi.nlm.nih.gov/pubmed/19863254

Location on Human Genome Now Associated With Memory

With a recent analysis of genomic data and memory test results of over 14,000 older adults a location of the human genome has been identified to relate to better memory performance which was not associated with brain performance before. The gene known as FASTKD2, located on chromosome 2, revealed that better episodic memory resulted from a G nucleotide rather than the common A nucleotide. This change known as a single nucleotide polymorphism was also connected to a larger hippocampus, a brain structure involved with storing and retrieving memory, and increased gray dense matter in the brain on magnetic resonance imaging scans.

Although, there is no claim that this is the gene which is solely responsible for memory but the hopes of this information is that the FASTKD2 gene could be targeted to help those with conditions such as Alzheimer's disease. A decline in memory and hippocampal atrophy are two of the main symptoms which are associated with Alzheimer's therefore the correction of those symptoms by targeting the FASTKD2 gene is where research is now heading.

This was especially interesting to me because it is a new, and genetic, solution to attempting to treat Alzheimer's. There have been a lot of suggestions of what can help prevent or prolong the effects of Alzheimer's but now with a new approach there is an attempt to help treat as well. I also just found it intriguing that memory could be found to be associated with a specific gene, although it is not a single gene responsible for memory.
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Algal Virus ATCV-1 Affects humans

A virus common in algae, known as ATCV-1, has been revealed to also infect humans. This virus, it turns out, has the ability to slow mammal brain function and limit attention span. A study at Johns Hopkins University School of Medicine did a study and found the virus in nearly half of them. That infected half also performed 10% worse on cognitive tests.

Researchers injected mice with the virus, and the newly infected mice took up to 10% longer to finish mazes and spent about 20% less time exploring new surroundings than their uninfected counterparts.
The researchers examined the each infected mouse's hippocampus and found that the virus had affected about 1300 genes in the mice, some of which are crucial to brain function, immune responses, and reactions to dopamine.

Whether or not the general public needs to worry about this virus is still unknown, but these findings open up several figurative rabbit-holes as to the safety of horticulturists. As of now, the consensus is that little to no diseases may be transmitted from plants to humans, but this may change very, very soon.

http://news.sciencemag.org/biology/2014/10/algal-virus-found-humans-slows-brain-activity

Two Scientists incorporate False Memories into Mouse

          Scientists Steve Ramirez and and colleague Xu Liu of MIT have stumbled upon a breakthrough in the study of Neuroscience. The mouse was placed on top of a small metal box which would cause a shock as soon as a pressure was felt. The mouse instantly jumped back, which is an expected fear response. however, the breakthrough is that the action never happened. The mouse never previously jumped on the metal box to learn the pain of the shock. The scientists added this false memory of pain when stepping on the box. So what does this mean?

                                         Picture from: http://fooyoh.com/geekapolis_gadgets_wishlist/7407700
                                       
            The specific brain cells can actually be manipulated to form a memory that never happened. This groundbreaking research can actually lead to figuring out new treatments for Alzheimer's disease or any other disease. What Ramirez and Liu specifically manipulated is the cluster of neurons known as the engrams. These cluster of neurons are where individual memories are stored. They devised methods to explore living brain actions which lead to the mice experiment and eventually these results. The part of the mice brain, called the hippocampus, was manipulated with a light sensitive protein called channelrhodopsin-2. The proteins in the hippocampus (gyrus proteins) would then be accustomed to the light sensitive protein incorporated in them.
        Next, the false memory was implemented. The results are outstanding. I believe this could lead to huge breakthroughs in the medical field. Also, if removing memories and replacing them is possible, is this a cure for neurological deiseases? maybe a cure for depression? Questions and actions are endless.

Article: http://www.smithsonianmag.com/innovation/meet-two-scientists-who-implanted-false-memory-mouse-180953045/?all&no-ist
Related Page: http://neurosciencenews.com/neuroscience-terms/memory-engrams/

Turmeric Compound Helps Regenerate Brain Stem Cells

Researchers in Germany recently discovered a bioactive compound in turmeric that promotes stem cell proliferation and differentiation. The study was conducted at the Institute of Neuroscience and Medicine in Julich. Researchers looked at the effects of aromatic aromatic-turmerone on endogenous neutral stem cells known as NSC. These stem cells are found in the adult brain. NSC plays an important role in self-repair and recovery of brain function in neurodegenerative diseases. 

Tumeric Powder, a commonly used spice, encompasses the compound Turmerone,
which holds regenerative neurological abilities.  

The researchers looked at the effect ar-turmerone had on NSC both in-vitro and vivo. NSC from Rat fetal was cultured over a seventy-two hour period in the presence of ar-turmerone. At certain concentrations of ar-turmerone, NSC proliferated 80% more than NSC cultured without the presence of ar-turmerone. The result also accelerated cell differentiation and did not yield any effect on cell death. To test in vivo, researchers injected adult rats with ar-turmerone. The study found that the subventricular zone and the hippocampus expanded. Both areas in mammalian brains are known for neurogenesis, the area where neurons grow. According to lead author, Adele Rueger, this is a major goal for regenerative medicine.
My culture commonly uses turmeric powder in many of our dishes. It's interesting to find out something I eat regularly has such amazing natural medicine indications. This is very promising news for the field of medicine. Considering the effects of ar-turmerone on NSC, the possibility of using ar-turmerone as a possible treatment for neurological disorders has suddenly increased through this study. Hopefully, the new findings are incorporated into future projects in regards to such disorders such as Alzheimer’s disease, which is becoming more prevalent as the years go one. 

Article: http://blogs.naturalnews.com/new-study-turmeric-compound-activates-regeneration-brain-stem-cells/

Article Related: Hippocampus - http://neuroscience.uth.tmc.edu/s4/chapter05.html

New Drugs May Transform Downs Sydrome

     The article from Scientific America talks about how geneticist, Roger Reeves and his team from Johns Hopkins University have conducted research that may lead towards pharmacological treatments for Down syndrome. Down syndrome is a genetic condition that is caused by an extra copy of chromosome 21 and the over expression of several genes on that chromosome which cause developmental delay leading to impaired learning, memory, and motor skills. Another characteristic of Down syndrome is that the cerebellum is is found to be 40% and is responsible for motor functions, motor learning, and balance.
     Down syndrome was initially thought to be incurable until Reeves and his team began experimenting on mice. They injected the mice with a chemical that stimulates an important neurodevelopmental pathway which stimulates cerebellum growth. Once doing this they found that they had not only "fixed" the cerebellum in mice but three months later they were able to complete a water maze. Such a task would usually thought to be predominantly controlled by the hippocampus so the researchers are still unsure whether they "inadvertently repaired" the hippocampus or if the cerebellum is actually responsible for more than what has been previously thought. 
     This type of treatment given to humans is thought to allow those with Down syndrome to live more independent lives. I think that these results are very exciting not only from a genetics standpoint and those who are affected by Downs but from the viewpoint that there is a hope of finding "cures" or treatments for other similar disabilities. Despite the excitement, I think we also need to consider being cautious in our evaluations of this research because sometimes research from animals fail to translate over to humans.

Article Link: http://www.scientificamerican.com/article/new-drugs-may-transform-downs-syndrome/

Info on Down syndrome: http://www.ndss.org/Down-Syndrome/What-Is-Down-Syndrome/

Stem Cell Transplant Restores Memory, Learning in Mice

An article in Science Daily describes a study at the University of Wisconsin-Madison. It is here where is has been shown that human stem cells can successfully implant themselves in the brain and then heal neurological deficits, says senior author Su-Chun Zhang, a professor of neuroscience and neurology. After the transplant, the mice scored significantly better on common tests of learning and memory in mice. To control for the damage in the brain in the experiment in the mice, the mice brain's were manipulated and deliberated damaged in the part that is involved in learning and memory.

The transplanted cells were then placed in the hippocampus,at the other end of those memory circuits. After the transferred cells were implanted, in response to chemical directions from the brain, they started to specialize and connect to the appropriate cells in the hippocampus, which is extremely significant. For more on the hippocampus, check out this sight :)

Even though this being a possibility in humans is a longggg way off, it is still crazy to think that this one day might be a possibility. The potential implications for people with brain damage or dementia is exciting, if this is transferable to humans!

 

 

 

The fruit fly helps with memory

Sciencedaily shared a journal’s article, ‘Frontiers in Neural Circuit’ about a new discovery using fruit flies to help in future therapies for memory and learning issues. The scientists at the University of Bristol studied the molecular changes in the hippocampus, which is the part of the brain that helps with learning. People make memories when calcium enters the brain cells and activates the enzyme Ca2+ responsive kinase to trigger a switch to keep it going until the calcium runs out. This whole process is known as Long Term Potentiation also referred to as the molecular memory switch. At first the big mystery was what triggers the chemical process in the brain to allow people to learn and make long term memories. The research team at the university executed experiments that temporarily disabled drosophila’s memory, and identified a gene, CASK, to be the synaptic molecule that regulated the memory switch

The team’s lead author mentioned that fruit flies were extremely compatible for the particular study because their neuronal functions and responses are similar to humans. The human CASK gene is 80% identical to the fruit flies’ same gene. The research team discovered that the drosophila’s memory formation was interrupted if they did not have the genes. Also, in humans mutations of this gene has been associated with learning difficulties. The finding of CASK’s ability provides a new way for therapies that reverse the effects of memory loss, and how the use of fruit flies’ still benefit in finding out more about diseases.

http://www.medicalnewstoday.com/releases/258409.php

Memory in Adults Impacted by Versions of Four Genes

Two studies have been done, led by Charles DeCarli, which may help prevent Alzheimer’s disease from occurring. In the first study, the hippocampus was targeted for the cause of memory loss because it shrinks as a person gets older. The gene variant that was identified caused the hippocampus to not have a defense against memory loss, which caused destruction and shrinkage. The risk of Alzheimer’s doubles every five years starting at the age of sixty-five. The gene that was identified as the main reason for shrinking were genes involved in maturation of the hippocampus and apoptosis, or cell death. By studying the normal regulations of the proteins causing hippocampus shrinkage, researchers are hoping to stop premature shrinkage. Different versions of a gene usually come down to changes in just one of the tens of thousands of DNA "letters" that make up genes. These one-letter differences are known as single-nucleotide polymorphisms, or SNPs. The experiment involved 9,232 dementia-free people over 67. The experiment showed four different genes that coded for hippocampus shrinkage. One gene, rs7294919, was strongly linked to hippocampus decline and health. In the second experiment, was aimed to deal with intracranial volume, which is an indirect measure of the size of the brain at full development. The experiment involved 8,175 elderly people. As a result, there was no association with brain volume. Though, they did discover that intracranial volume was associated with two loci: rs4273712, a known height locus on chromosome 6q22, and rs9915547, tagging the inversion on chromosome 17q21. Using these two studies, researchers hope to delay memory loss in older people, and reduce the number of Alzheimer’s cases.