作者: Lucas Bortolotto Rizzo , Leonardo Gazzi Costa , Rodrigo B. Mansur , Walter Swardfager , Síntia Iole Belangero
DOI: 10.1016/J.NEUBIOREV.2014.02.004
关键词:
摘要: Bipolar Disorder (BD) has been conceptualized as both a cyclic and progressive disorder. Mechanisms involved in neuroprogression BD remain largely unknown although several non-mutually exclusive models have proposed explanatory frameworks. In the present paper, we propose that pathophysiological changes observed (e.g. brain structural alterations, cognitive deficits, oxidative stress imbalance, amyloid metabolism, immunological deregulation, immunosenescence, neurotrophic deficiencies telomere shortening) converge on model of accelerated aging (AA). Aging can be understood multidimensional process involving physical, neuropsychological, social changes, which highly variable between individuals. Determinants successful (e.g environmental genetic factors), may also confer differential vulnerability to components pathophysiology contribute clinical presentation BD. Herein discuss how understanding senescence search for new promising molecular targets explain ameliorate We strengths limitations this concept.