Abstract
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive atrophy of neurons especially in the cerebral cortex and hippocampus, reducing the loss of synapses and neuronal plasticity, the finding of extracellular deposits of amyloid β (Aβ) in senile plaques and the presence of intracellular neurofibrillary tangles (NFT). There are two different basic forms of AD: (1) Familial form manifested among 40th to 60th year of age, at which the majority of the cases associated with rare, high penetrant mutations in three genes: the gene for amyloid precursor protein, APP, presenilin gene 1, PSEN1 and presenilin 2 gene, PSEN2 and (2) late (" late -onset AD, LOAD "), also called sporadic form.
LOAD is now at least 90 % of all cases of AD and its incidence is increasing, probably in connection with the growing importance of adverse environmental factors. LOAD pathogenesis is not yet elucidated, is applied here oxidative stress, inflammation, and metabolic factors, many of which are in the foreground variations in the metabolism of lipid substances, which, given the representation of lipids in the central nervous system (CNS) is not surprising.
This includes in particular disorder transformations of sterols, sphingolipids and glycerophospholipids. U LOAD applies a complex interaction of genetic and environmental factors.
The most important genetic risk factors associated with the occurrence LOAD is the APOE gene, respectively the presence of allele ε4. Important risk factors are also particularly age, obesity, high caloric intake and saturated fats in the diet, cigarette smoking, diabetes mellitus type 2 (DM2), hyperhomocysteinemia, or depression.