Alzheimer’s disease is attributed to a slow breakdown of neuronal networks throughout the brain. It may begin in the mid-brain level in an area called the hippocampus. A neuronal network may be dedicated to a scene (person, animal, place), sound, taste, smell, touch. In conjunction with other neuronal networks, these help form your reality. Alzheimer disease interferes and destroys these networks. There are several hypotheses as to why and how this happens. A group of researchers at the University of California San Francisco have detected a gene variant among Alzheimer brains and are studying its use to find causes and a cure of Alzheimer disease.
Alzheimer disease apoE4 genetic cure? Studies published in April 2018 show positive indicators that a gene variant of APOE4 may be associated with beta-amyloid fragments and plaque found in those diagnosed as dementia/Alzheimer disease.. There are many kinds of memory loss coming from many sources. Alzheimer is seemingly over-diagnosed and is not limited to an older population. This APOE4 genetic variant may be only a piece of a very large puzzle. Alzheimer disease is not a game. It’s very serious. Yet, inferences of causality and treatment of those are ethereal – like gases.
The APOE gene set provides instructions for making a protein called apolipoprotein E. This protein combines with fats (lipids) in the body to form molecules called lipoproteins. Lipoproteins are responsible for packaging cholesterol and other fats and carrying them through the bloodstream. One of these APOE4 genes might lead to a pathway to cure Alzheimer’s disease, a cognitive memory disorder.
Scientists in an independent San Francisco lab believe that an apoE4 gene detection may be a pathway toward curing Alzheimer’s disease.
Alzheimer disease is a diagnosis within the category of dementia. Alzheimer is usually found on brain examinations after death. New tests, such as MRI, PET, and Tau help physicians study potential possibilities to infer exact causes. Complicating an Alzheimer disease diagnosis is that both dementia and Alzheimer is a neurodegenerative disease, which means there is progressive brain cell death that happens over time. In a person with Alzheimer’s, the tissue has fewer and fewer nerve cells and connections.
For example, I was part a study on REM-Dream Sleep and cerebral memory storage. During REM, there is a switch among 2 neurotransmitters – acetylcholine and nor-epinephrine. Dreaming helps store long-term memories and associations. REM dreaming involves bringing acetylcholine up to the cortex to help store these memories. Theory was that if normal REM did not occur, long term memories would not be stored. This remains one of a dozen possible theories of a possible inference of dementia toward Alzheimer.
There have been research observations between schizophrenia and Alzheimer disease in that a certain area of the brain may be cause for both. Alzheimer’s disease and schizophrenia are radically different disorders, new research suggests that each disorder affects the same areas of the brain. Scientists observed similar lesions near the brain’s pre-frontal cortex.
A more current hypothesis are the development of beta-amyloid plaques and tangles to (and within) the brain. These could disassociate memory linkages. These are found in results of MRI and PET scans. The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. By disrupting neuronal network interaction, formation of these beta-amyloid proteins and peptides (over time) may result on Alzheimer disease symptoms.
Beta-amyloid is an important peptide, an amino acid chain from a host protein.. It does leave fragments between neurons that can form plaques. A normal brain, however, can eliminate beta-amyloid fragments before they disrupt neuron transmissions. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells. Beta-amyloid is chemically “sticky” and gradually builds up into plaques.
Based on the beta-amyloid hypothesis and APOE44 variants, there are tests available to determine if you have these APOE4 gene variants. It is not FDA approved and is not concise at determining whether or not you may get Alzheimer disease. It may cause more worry than calm. APOE4 has been behind diagnoses such as high-cholesterol, coronary artery diseases, and obesity. Can APOE4 variants be used to treat, cure, or detect Alzheimer disease with some accuracy?
Could something as nasty as APOE4 variations help treat dementia and aging? Who knows? Potentially there may be other genes and other proteins? Nutritionists believe that diets rich in these foods may help reduce beta-amyloid build-up:
Foods That Reduce Your Alzheimer’s Risk
Walnuts (and almonds, pecans, hazelnuts) Walnuts might be small in size, but they pack a big nutritional punch.
Salmon (and mackerel, sardines, other fatty fish) …
Spinach (and kale, other leafy greens)
In March 2018, the president signed into law a $414 million increase for Alzheimer’s and dementia research funding at the National Institutes of Health (NIH) and Kevin and Avonte’s Law, important legislation to protect those who wander. Alzheimer disease is getting everyone’s attention.
The dilemma is how valid this Beta-Amyloid hypothesis is, and how solid the apoE4 genetic cure for Alzheimer disease might be. As most early studies indicate, further research is necessary.