Adult Neurogenesis: A Potential Tool for Early Diagnosis in Alzheimer's Disease?

Alzheimer's disease (AD) is a devastating age-related neurodegenerative disorder characterized by progressive impairment of cognition and short-term memory loss. The deposition of amyloid-beta (A beta) 1-42 into senile plaques is an established feature of AD neuropathology. Controversy still exists about the amyloid pathway as the initiating mechanism or a mere consequence of the events leading to AD. Nevertheless, A beta toxicity has been probed in vitro and in vivo and increased production or decreased clearance of A beta peptides are reported to play a major role in the development of AD. Treatment of neural stem cells with A beta in vitro induces neuronal differentiation. Increased neurogenesis has been also described in AD patients as well as in amyloid-beta protein precursor (A beta PP) transgenic mice. Adult neurogenesis is greatly enhanced in young A beta PP transgenic mice, before other AD-liked pathologies, and reduced in older animals. This increased neurogenesis at young ages might be the first pathology related to AD, which is detectable long before other harmful manifestation of the disease. Therefore, understanding the mechanisms of A beta-induced neurogenesis will reveal insights into the pathogenesis of AD and may prove useful as an early AD biomarker.