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Home » Biology Articles » Neurobiology » Molecular & Cellular Neurobiology » Amyloid beta, neural lipids, cholesterol & Alzheimer's disease » Posing the problem

Posing the problem
- Amyloid beta, neural lipids, cholesterol & Alzheimer's disease

Since 1966 more than one hundred thousand research papers were devoted to cholesterol and only few articles dealt with the role of cholesterol in neuronal function, synaptic plasticity and neurodegeneration (according to the PubMed and HighWire Press search engines). This mysterious molecule is accused in atherosclerosis and heart disease, but was largely understudied in relation to brain function and neural structural and functional (i.e. activity dependent) plasticity. Living cells (including neurons and glial cells) produce their own cholesterol and can receive or donate cholesterol via lipoprotein transit, an attested body lipid transportation system. This system operates a number of vehicle classes, including well-known (and considered to be “bad”) LDLs and “good“ HDLs [1, 2]

Apart from this whole-body-system stands distinct brain lipid transport authority that uses different subtypes of HDLs and normally does not maintain LDLs [3]. This vital service is in charge of cholesterol redistribution inside the brain and cholesterol export out of the brain border to liver for excretion. There is no reported cholesterol import to the brain, an issue that makes brain cholesterol availability entirely dependent on local manufacturing. Brain lipid transportation must have good management and operating capacity, because the quantity of cholesterol in the brain is much higher then anywhere else in the rest of the body. Thus, having just two percent of the body weight, brain has a quarter of cholesterol present in the whole individual.

Conceivable, the break in any element of the harmonized system of brain/neuronal cholesterol transport (caused by genetic defects of one of the enzyme or receptor associated with cholesterol turnover; by pharmacological modulation or environmentally) may result in abnormal homeostasis of cholesterol in the brain and impair fine tuning of synaptic function (see online Refs. 2, 3, 4 for instant access to detailed bibliography).

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