Elsevier Logo It is predicted that by 2050, the world will encompass around 80 million people diagnosed with Alzheimer’s disease. Unique investigations and experiments can probably help decline this number. A latest research undertaken by the Laboratory of Psychiatry and Experimental Alzheimers Research at the Medical University Innsbruck (Austria) asserts that chronic high fat cholesterol diet develops pathologies similar to Alzheimer’s disease.

Extracellular aggregates (plaques) of the small peptide beta-amyloid, hyperphosphorylation of the protein tau and subsequent formation of intracellular neurofibrillary tangles, degeneration of neurons secreting the neurotransmitter acetylcholine, inflammation, as well as cerebrovascular dysfunction apparently are major pathological hallmarks of Alzheimer’s disease. Though the actually cause of Alzheimer’s is not known, it is suspected that dysregulation of amyloid-precursor protein expression and beta-amyloid clearance are involved. Another hypothesis suggests that a pathological cascade of events results in hyper-phosphorylation of tau.

According to the third hypothesis, chronic long-lasting mild cerebrovascular damage, such as inflammatory processes and oxidative stress lead to Alzheimer’s. The condition probably develops 20-30 years before first symptoms appear. The present investigation was initiated for analyzing the effects of hypercholesterolemia in adult rats. Dr. Christian Humpel lead investigator of the research and colleagues fed male 6 months old Sprague Dawley rats with normal food or a special 5 percent cholesterol-enriched diet. The normal diet eating group was regarded as controls and those on cholesterol-enriched food were hypercholesterolemia.

On completion of 5 month researchers scrutinized animals for behavioral impairments and pathological markers identical to those observed in the brains of Alzheimer’s patients. It was concluded that chronic hypercholesterolemia may give rise to memory impairment, cholinergic dysfunction, inflammation, boosted cortical beta-amyloid and tau as well as induced microbleedings. All these markers possibly resemble an Alzheimer’s disease-like pathology. It was mentioned that since Alzheimer’s is a complex heterogeneous disease, it’s difficult to assert that cholesterol alone results in the disease.

The research was published in Molecular Cellular Neuroscience.