Neurotrophins and Other Growth Factors in the Pathogenesis of Alzheimer's Disease

The involvement of the changed expression/function of neurotrophic factors in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD), has been suggested. AD is one of the age-related dementias, and is characterized by cognitive impairment with decreased memory function. Developing evidence demonstrates that decreased cell survival, synaptic dysfunction, and reduced neurogenesis are involved in the pathogenesis of AD. On the other hand, it is well known that neurotrophic factors, especially brain-derived neurotrophic factor (BDNF) and its high-affinity receptor TrkB, have multiple roles in the central nervous system (CNS), including neuronal maintenance, synaptic plasticity, and neurogenesis, which are closely linked to learning and memory function. Thus, many investigations regarding therapeutic approaches to AD, and/or the screening of novel drug candidates for its treatment, focus on upregulation of the BDNF/TrkB system. Furthermore, current studies also demonstrate that GDNF, IGF1, and bFGF, which play roles in neuroprotection, are associated with AD. In this review, we introduce data demonstrating close relationships between the pathogenesis of AD, neurotrophic factors, and drug candidates, including natural compounds that upregulate the BDNF-mediated neurotrophic system.

Automated summary

The change in expression/function of neurotrophic factors is implicated in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). AD is an age-related dementia characterized by cognitive impairment and decreased memory function. Decreased cell survival, synaptic dysfunction, and reduced neurogenesis are involved in AD pathogenesis. Many investigations focus on upregulating the BDNF/TrkB system as a therapeutic approach to AD.