Brain-derived neurotrophic factor in Alzheimer's disease and its pharmaceutical potential

Synaptic abnormalities are a cardinal feature of Alzheimer's disease (AD) that are known to arise as the disease progresses. A growing body of evidence suggests that pathological alterations to neuronal circuits and synapses may provide a mechanistic link between amyloid beta (A beta) and tau pathology and thus may serve as an obligatory relay of the cognitive impairment in AD. Brain-derived neurotrophic factors (BDNFs) play an important role in maintaining synaptic plasticity in learning and memory. Considering AD as a synaptic disorder, BDNF has attracted increasing attention as a potential diagnostic biomarker and a therapeutical molecule for AD. Although depletion of BDNF has been linked with A beta accumulation, tau phosphorylation, neuroinflammation and neuronal apoptosis, the exact mechanisms underlying the effect of impaired BDNF signaling on AD are still unknown. Here, we present an overview of how BDNF genomic structure is connected to factors that regulate BDNF signaling. We then discuss the role of BDNF in AD and the potential of BDNF-targeting therapeutics for AD.

Automated summary

Synaptic abnormalities are a key aspect of Alzheimer's disease, connecting pathological changes to cognitive impairment. Brain-derived neurotrophic factors are crucial in synaptic plasticity for learning and memory, and have potential as diagnostic biomarkers and therapeutic molecules for AD. The exact mechanisms underlying the effects of impaired BDNF signaling on AD are still unclear.