{'fraction_non_alphanumeric': 0.023931623931623933, 'fraction_numerical': 0.0, 'mean_word_length': 6.506410256410256, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Brain-derived neurotrophic factor: a mediator of inflammation-associated neurogenesis in Alzheimer’s disease

Abstract In early- or late-onset Alzheimer’s disease (AD), inflammation, which is triggered by pathologic conditions, influences the progression of neurodegeneration. Brain-derived neurotrophic factor (BDNF) has emerged as a crucial mediator of neurogenesis, because it exhibits a remarkable activity-dependent regulation of expression, which suggests that it may link inflammation to neurogenesis. Emerging evidence suggests that acute and chronic inflammation in AD differentially modulates neurotrophin functions, which are related to the roles of inflammation in neuroprotection and neurodegeneration. Recent studies also indicate novel mechanisms of BDNF-mediated neuroprotection, including the modulation of autophagy. Numerous research studies have demonstrated reverse parallel alterations between proinflammatory cytokines and BDNF during neurodegeneration; thus, we hypothesize that one mechanism that underlies the negative impact of chronic inflammation on neurogenesis is the reduction of BDNF production and function by proinflammatory cytokines.