“The molecular mechanisms accounting for the environmental risk factor stimulation of Alzheimer’s disease (AD) pathogenesis including traumatic brain injury, diabetes, and chronic cerebral hypoperfusion remain unclear. The BDNF/TrkB signaling pathway plays a critical role in neuronal synaptic plasticity and neuronal survival. Since the BDNF/TrkB pathway is reduced during aging and in AD human brains, we hypothesize that the crosstalk between these risk factors and BDNF/TrkB deficiency may mediate AD pathologies. Our previous studies establish that the C/EBPβ/δ-secretase pathway plays a pivotal role in triggering the major AD pathologies. Therefore, in the current report, we provide extensive evidence demonstrating that BDNF/TrkB reduction regulates this pathway activation under various risk factors, mediating Aβ and Tau pathology spreading in the brain.”


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