How to (not) lose your mind — a (not so) original approach on Alzheimer’s disease (1)

in Proof of Brain2 months ago

I will start a new series in here about Alzheimer's disease, and how to delay the inevitable, by prevent it before it happens. Please note that many of the researches mentioned in here are still in experimental phase, and more than often, there is not enough data to reach clear conclusions.

Did you know that Alzheimer’s disease is in fact not one but a group of three diseases. Type one (inflammation type) is characterized by loss of ability to store new information, but the long term memory and the ability to speak, calculate, spell and write is retained. Type 2 is characterized by loss of trophic support, and by loss of ability to store new information, but the long term memory and the ability to speak, calculate, spell and write is retained. Inflammatory markers are not high in this case, they can even be lower than normal. You can have both type 1 and type 2 in the same time later in life. This may run in the family. Type 3 is toxic (vile) and appears usually in people carrying the common ApoE3 allele rather than ApoE4. Does not run in the family. Usually strikes at age 40–50, following grat stress, with cognitive difficulties involving numbers , speech and organizing skills. Short term, long term and procedural memory (how to do simple or complex things) is affected. Exposure to toxic compounds (heavy metals, mycotoxins from mold) seems to be also one of the factors increasing the risk.

Type 1 starts at age 40–50 if you have one copy of ApoE4 allele, or at age 50–60 if you have two copies of ApoE4. No copies of ApoE4 — starts around 60–70. Type 2 initiates a decade later than type one, given the same variation of ApoE4.

(Extra information here — Apolipoprotein E (APOE) is a protein involved in the metabolism of fats in the body. It is implicated in Alzheimer’s disease and cardiovascular disease. ApoE3 is considered the “neutral” APOE genotype. ApoE4 has been implicated in atherosclerosis, Alzheimer’s disease, impaired cognitive function,reduced hippocampal volume, HIV, faster disease progression in multiple sclerosis, unfavorable outcome after traumatic brain injury, ischemic cerebrovascular disease, sleep apnea, accelerated telomere shortening and reduced neurite outgrowth.A notable advantage of the E4 allele (relative to E2 and E3) is a positive association with higher levels of vitamin D, which may help explain its prevalence despite its seeming complicity in various diseases or disorders. APOE transports lipids, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood. It is synthesized principally in the liver, but has also been found in other tissues such as the brain, kidneys, and spleen. In the nervous system, non-neuronal cell types, most notably astroglia and microglia, are the primary producers of APOE, while neurons preferentially express the receptors for APOE. There are seven currently identified mammalian receptors for APOE which belong to the evolutionarily conserved LDLR family. Hence the relation with the amyloid-beta plaque issue in Alzheimer’s disease).

I will write a bit more about this soon.

Take care and be safe!

All the best,

George

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This post was published initially on https://mihalachecatalin.medium.com/






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