Calcium and Neurogenesis in Alzheimer's Disease

Jun Ming Wang,Chenyou Sun

doi:10.3389/fnins.2010.00194

Abstract

It was evidenced that impairment of calcium homeostasis is a potential mechanism in the development of Alzheimer's disease (AD). It remains, however, unclear how the calcium signaling are associated with in AD progression. Here we review recent studies to discuss the relationship among the signaling of intracellular calcium concentration, neurogenic activity, and AD progression. Analyzing these findings may provide new ideas to improve the neurogenic status in pathological processes in the aging brain.

Highlights

Alzheimer’s disease (AD) is the most common form of dementia involving slowly developing, fatal neurodegeneration with massive brain atrophy especially in the medial temporal lobe, including the hippocampus (Hardy, 2006; Haass and Selkoe, 2007; Wang et al, 2007)
AD is pathologically characterized by the presence of cerebral senile plaques containing extracellular deposits of β-amyloid peptide (Aβ) from the amyloid precursor protein (APP), the accumulation of intraneuronal neurofibrillary tangles (NFTs) containing hyperphosphorylated tau protein, dysfunction of synapses, and loss of neurons (Mattson, 2004; Hardy, 2006)
It have been reported that transient [Ca2+]i increases within the neural progenitor cells (NPC) is triggered by a neurosteroid, allopregnanolone, which is a GABAA receptor modulator, and is mediated by a voltage-gated calcium channel

Summary

Introduction

Alzheimer’s disease (AD) is the most common form of dementia involving slowly developing, fatal neurodegeneration with massive brain atrophy especially in the medial temporal lobe, including the hippocampus (Hardy, 2006; Haass and Selkoe, 2007; Wang et al, 2007). Accumulated data indicated that transient increase of intracellular calcium concentration ([Ca2+]i) may facilitate the neurogenesis (Dayanithi and Tapia-Arancibia, 1996; Wang and Brinton, 2008).

Results

Conclusion