When neurogenesis encounters aging and disease |
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| Authors: | Lazarov Orly Mattson Mark P Peterson Daniel A Pimplikar Sanjay W van Praag Henriette |
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| Institution: | 1 Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA;2 Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD, USA;3 Center for Stem Cell and Regenerative Medicine and Department of Neuroscience, The Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA;4 Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA |
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| Abstract: | In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits and impairments in disorders such as Alzheimer's disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and β-amyloid probably contribute to impaired neurogenesis in AD. Because factors such as exercise, environmental enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seems promising. |
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