Neurology Central

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

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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