Author: Reese, Lindsay C.; Taglialatela, Giulio
Description: Alzheimer’s disease (AD) is an incurable age-related neurodegenerative disorder characterized by profound memory dysfunction. This bellwether symptom suggests involvement of the hippocampus — a brain region responsible for memory formation — and coincidentally an area heavily burdened by hyperphosphorylated tau and neuritic plaques of amyloid beta (AB). Recent evidence suggests that pre-fibrillar soluble AB underlies an early, progressive loss of synapses that is a hallmark of AD. One of the downstream effects of soluble AB aggregates is the activation of the phosphatase calcineurin (CaN). This review details the evidence of CaN hyperactivity in ‘normal’ aging, models of AD, and actual disease pathogenesis; elaborates on how this could manifest as memory impairment, neuroinflammation, hyperphosphorylated tau, and neuronal death.
Subject headings: Alzheimers disease; Amyloid beta; Calcineurin; Calcium; Brain
Publication year: 2011
Journal or book title: Current Neuropharmacology
Volume: 9
Issue: 4
Pages: 685-692
Find the full text: https://www.strategian.com/fulltext/Reese2011.pdf
Find more like this one (cited by): https://scholar.google.com/scholar?cites=14180598413970109114&as_sdt=5,26&sciodt=0,26&hl=en
Serial number: 3395