Neuronal survival promotion

Neuronal survival promotion is a biological process and a central therapeutic objective in neurology rather than a single molecular target or receptor. It describes the physiological mechanisms that maintain the viability of neurons and protect them against programmed cell death, or apoptosis, particularly under conditions of oxidative stress, excitotoxicity, or protein aggregation [PMID: 25685415]. This process is largely governed by neurotrophic factor signaling, specifically via the Brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, Tropomyosin receptor kinase B (TrkB), which trigger intracellular survival cascades like the PI3K/Akt pathway [NCBI: NBK557602]. In the context of drug development, promoting neuronal survival is a primary strategy for treating chronic neurodegenerative conditions such as Alzheimer's and Parkinson's diseases, as well as acute injuries like stroke and spinal cord trauma [PubMed: 31054234]. Various pharmacological agents aim to mimic or enhance these survival signals to slow disease progression and preserve cognitive or motor functions. Because 'neuronal survival promotion' refers to a broad functional outcome involving multiple interconnected pathways and proteins, it is classified as a biological process rather than a discrete drug target entity in biochemical databases [StatPearls: NBK507844].

Other names

NeuroprotectionPromotion of neuronal survivalNeuronal maintenanceNeuronal rescue

Neuronal survival promotion is achieved through the activation of endogenous neuroprotective pathways, such as the PI3K/Akt and MAPK/ERK signaling cascades, which inhibit pro-apoptotic proteins and stabilize mitochondrial integrity. Drugs targeting this process often act as agonists for neurotrophin receptors (e.g., TrkB), scavengers of reactive oxygen species, or inhibitors of glutamate-induced excitotoxicity to prevent calcium-mediated cell death.