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Calcium dysregulation in Alzheimer's disease.

Abstract：

:Alzheimer disease (AD) is the most common form of adult dementia. Its pathological hallmarks are synaptic degeneration, deposition of amyloid plaques and neurofibrillary tangles, leading to neuronal loss. A few hypotheses have been proposed to explain AD pathogenesis. The beta-amyloid (Abeta) and hyperphosphorylated tau hypotheses suggest that these proteins are the main players in AD development. Another hypothesis proposes that the dysregulation of calcium homeostasis may be a key factor in accelerating other pathological changes. Although Abeta and tau have been extensively studied, recently published data provide a growing body of evidence supporting the critical role of calcium signalling in AD. For example, presenilins, which are mutated in familial cases of AD, were demonstrated to form low conductance calcium channels in the ER and elevated cytosolic calcium concentration increases amyloid generation. Moreover, memantine, an antagonist of the NMDA-calcium channel receptor, has been found to have a beneficial effect for AD patients offering novel possibilities for a calcium signalling targeted therapy of AD. This review underscores the growing importance of calcium ions in AD development and focuses on the relevant aspects of calcium homeostasis.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Bojarski L,Herms J,Kuznicki J

doi

10.1016/j.neuint.2007.10.002

subject

Has Abstract

pub_date

2008-03-01 00:00:00

pages

621-33

issue

4-5

eissn

0197-0186

issn

1872-9754

pii

S0197-0186(07)00289-6

journal_volume

52

pub_type

杂志文章,评审

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