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Brain-derived neurotrophic factor (BDNF) is a critical neurotrophin that supports the survival of existing neurons and encourages the growth and differentiation of new neurons and synapses [1, 2]. It acts primarily through the high-affinity Tropomyosin receptor kinase B (TrkB) and the low-affinity p75 neurotrophin receptor (p75NTR) to modulate synaptic plasticity and long-term potentiation, which are fundamental to learning and memory [3, 5]. In the clinical context, reduced BDNF levels are strongly associated with the pathophysiology of major depressive disorder and neurodegenerative conditions like Alzheimer's and Huntington's disease [3]. Many current neuropsychiatric treatments, such as SSRIs and ketamine, exert their therapeutic effects by indirectly increasing BDNF expression or signaling [4]. Direct targeting of the BDNF pathway via TrkB agonists or recombinant BDNF is an active area of drug development, though it faces significant hurdles regarding blood-brain barrier delivery and the maintenance of physiological signaling patterns [4, 5].
Activation of the Tropomyosin receptor kinase B (TrkB) signaling pathway or induction of endogenous BDNF gene expression.
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