{"title":"24 Adult Neurogenesis in Neurodegenerative Diseases","authors":"P. Brundin, J. Winkler, E. Masliah","doi":"10.1101/087969784.52.503","DOIUrl":null,"url":null,"abstract":"The neurodegenerative disorders parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease (AD), and human immunodeficiency virus (HIV)-associated cognitive impairment (HACI) all present with a gradual loss of relatively well-defined neuronal populations. Under all of these conditions, progression is slow. In some cases, the neuropathology is relatively restricted, leaving significant parts of the nervous system unaffected. They have therefore become interesting targets for restorative therapies. One of the most exciting ideas for repair is the concept that one might be able to harness the adult brain’s endogenous capacity for cell renewal. Thus, it might be possible to direct newborn cells in the adult brain to migrate to the regions affected by the disease and there differentiate into the specific types of neurons that succumb due to the disease (Jordan et al. 2006). This concept is based on the realization that the adult mammalian brain also has the capacity to generate new neurons. The interaction between neurogenesis in the adult brain and neurodegenerative disease can also be viewed from another angle. It is conceivable that failure of a normal reparative process, i.e., adult neurogenesis, contributes to the development of the disease. Taken to its extreme, this idea has even led to the hypothesis that the symptoms in some neurodegenerative diseases may partly be the consequence of reduced adult neurogenesis, resulting in a failed replacement of dying neurons (Armstrong and Barker 2001). The objectives of this chapter are to describe neurogenesis in the adult brain and to determine to what extent it is...","PeriodicalId":10493,"journal":{"name":"Cold Spring Harbor Monograph Archive","volume":"29 1","pages":"503-533"},"PeriodicalIF":0.0000,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cold Spring Harbor Monograph Archive","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/087969784.52.503","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3
Abstract
The neurodegenerative disorders parkinson’s disease (PD), Huntington’s disease (HD), Alzheimer’s disease (AD), and human immunodeficiency virus (HIV)-associated cognitive impairment (HACI) all present with a gradual loss of relatively well-defined neuronal populations. Under all of these conditions, progression is slow. In some cases, the neuropathology is relatively restricted, leaving significant parts of the nervous system unaffected. They have therefore become interesting targets for restorative therapies. One of the most exciting ideas for repair is the concept that one might be able to harness the adult brain’s endogenous capacity for cell renewal. Thus, it might be possible to direct newborn cells in the adult brain to migrate to the regions affected by the disease and there differentiate into the specific types of neurons that succumb due to the disease (Jordan et al. 2006). This concept is based on the realization that the adult mammalian brain also has the capacity to generate new neurons. The interaction between neurogenesis in the adult brain and neurodegenerative disease can also be viewed from another angle. It is conceivable that failure of a normal reparative process, i.e., adult neurogenesis, contributes to the development of the disease. Taken to its extreme, this idea has even led to the hypothesis that the symptoms in some neurodegenerative diseases may partly be the consequence of reduced adult neurogenesis, resulting in a failed replacement of dying neurons (Armstrong and Barker 2001). The objectives of this chapter are to describe neurogenesis in the adult brain and to determine to what extent it is...