A Role for Calcineurin in Alzheimers Disease

Title: A Role for Calcineurin in Alzheimers Disease

Volume: 9 Issue: 4

Author(s): Lindsay C. Reese and Giulio Taglialatela

Affiliation:

Keywords: Alzheimers, amyloid beta, calcineurin, calcium, pre-fibrillar soluble A, glycogen synthase kinase-3 beta (GSK-3 ), voltage-gated sodium (Na+), neurotransmitter, Ca2+ fluctuation

Abstract: Alzheimers 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 (Aβ). Recent evidence suggests that pre-fibrillar soluble Aβ underlies an early, progressive loss of synapses that is a hallmark of AD. One of the downstream effects of soluble Aβ 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.

Cite this article as:

C. Reese Lindsay and Taglialatela Giulio, A Role for Calcineurin in Alzheimers Disease, Current Neuropharmacology 2011; 9 (4) . https://dx.doi.org/10.2174/157015911798376316