Neurology Central

BACE1 levels are increased in plasma of Alzheimer’s disease patients compared with matched cognitively healthy controls

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In Alzheimer’s disease (AD), the amyloidogenic pathway results in the production of Aβ peptide from AβPP. Aβ has a hydrophobic nature and aggregates extracellularly, forming senile plaques [1]. In turn, neurofibrillary tangles are intracellular fibrillar aggregates of the hyperphosphorylated microtubule-associated Tau protein. Together, these entities are the key microscopic neuropathological hallmarks of AD [2].
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