As the entire human being works as a perfectly balanced whole, each and every disturbance at any level brings
other disturbances, like a chain reaction to superior levels, the current researches aim for the molecular aspects of any
physiological disorders. It is well possible that any physiological reaction is not the cause of a disease but an effect of
molecular disturbances in biochemical and genetic mechanisms responsible for a feature or behavior exhibit. The exact
causes of Alzheimer’s disease are mostly unknown, excepting 1 to 5% cases notably identified with obvious genetic
variance. In the scientific world, there are many hypotheses that explain the occurrence of Alzheimer’s disease: amyloidal
hypothesis, taupathy hypothesis, cholinergic hypothesis and so on, but from all of these it seems that the
molecular/genetic hypothesis is the most studied of all, because of its relevance to the true pathological mechanism. It
seems that some allelic variants and mutations of genes that encode important regulatory molecules in neuronal activity
may give a certain predisposition to Alzheimer’s disease or to other neurodegenerative diseases, even in young
individuals. One good example is the APOE gene that encodes a surface component of triglyceride reach lipoproteins. At
the neuronal level, this glycoprotein has an important role in lipid distribution during nerves growth and repair. The
APOE gene exists in three allele variants present in human population in different proportions (ε2, ε3, ε4) which in
different combinations give to the carrier various predispositions to cholesterol and triglycerides mechanisms disorders,
Levy’s bodies dementia and Alzheimer’s disease (ε4 allele