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clinmed/2001100005v1 (November 27, 2001)
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Brain cholesterol pathology is the cause of Alzheimer's disease

Alexei R. Koudinov, and Natalia V. Koudinova

Several recent reports provided important knowledge on how "inhibiting cholesterol production in the brain might inhibit amyloid b (Ab) production, and reduce the accumulation of Ab that causes Alzheimers disease (AD)". As we show and discuss here cholesterol homeostasis biological misregulation itself has a key role for synaptic plasticity impairment, neuronal degeneration and is the primary cause for several AD hallmarks not limited to brain amyloid. Moreover, Alzheimer's changes in neurochemistry of Ab, tau, neuronal cytoskeleton, and oxidative stress reactions likely represent physiological transitory mechanisms aiming to compensate impaired brain cholesterol dynamics and/or associated neurotransmission and synaptic plasticity failure.

Keywords: amyloid beta protein precursor, cholesterol, Down syndrome etiology, learning, lipid, memory, lipoprotein LDL LRP VLDL HDL receptor, LTP, neurodegeneration marker, neurofilament, NPC, oxidative stress, PHF NFT tau phosphorylation, peroxidation, phospholipids, plaque, therapy, synaptic plasticity, secretase, SREBP

E.mail: neurodegeneration{at}hotmail.com or koudin{at}imb.ac.ru


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Behind tau and amyloid beta in AD's pathogenesis.
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ClinMed NetPrints, 11 Jan 2002 [Full text]
Alzheimer's Disease Byophysical Semeiotics supports the pathophysiology of Koudiniv's theory.
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