Affiliations: School of Medicine, University of St Andrews, St Andrews, UK
Correspondence:
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Correspondence to: Alan J. Stewart, School of Medicine, University of St Andrews, Medical and Biological Sciences Building, North Haugh, St Andrews, KY16 9TS, UK. Tel.: +44 1334 463546; Fax: +44 1334 463482; E-mail: ajs21@st-andrews.ac.uk.
Abstract: Alzheimer's disease (AD) is associated with altered neuronal Ca2+ homeostasis. Ca2+ is known to accumulate in AD-affected neurons leading to deficits in neurological activity that are characteristic of the disease. This has led to the coinage of the term “calciumopathy”. However, the mechanisms of how and why Ca2+ levels are increased in the AD-affected brain remain unknown. Identifying these mechanisms is crucial for our ability to treat and understand the disease processes that are occurring. Recent work has revealed the existence of a novel signaling pathway that may contribute toward this calciumopathy. Phospholipase C-η enzymes have recently been implicated in the modulation and amplification of Ca2+ signals and are known to be expressed in neuronal regions of the brain associated with cognition and memory. In this article their potential impact on neuronal Ca2+ signaling and AD pathogenesis is discussed.
Keywords: Calcium, dementia, inositol 1, 4, 5-triphosphate, phospholipases, signal amplification
