A risk factor for the emergence of neurodegenerative illnesses is advancing age. Certain brain regions in various people are affected differently by age, with memory being the main area affected. Particularly in the older population, episodic memory is one of the most negatively impacted. The capacity of specific regions, such as the hippocampal dentate gyrus (DG), to produce new nerve cells is a type of plasticity that may aid in safeguarding the brain amid the ongoing process of aging. Particularly in the older population, the memory of everyday events is one of the most negatively impacted. The capacity of specific regions, such as the hippocampal dentate gyrus (DG), to produce new neurons is a type of plasticity that may aid in safeguarding the brain amid the ongoing process of aging.
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Administration of TGF-alpha
The adult brain exhibits neurogenesis during the course of an individual’s lifetime. The resulting neurons have an impact on cognitive functions including learning, memory, and pattern recognition. Several pieces of evidence demonstrate that adult hippocampal neurogenesis decreases with aging in mammals, including humans. This drop is accompanied by a decline in hippocampus-dependent cognitive capacities. Controlling NSC activation is crucial for the regulation of neuron creation within neurogenic niches. The development of treatments to stop the evolution of neurological problems in the elderly population may be facilitated by measures that promote neurogenesis in the DG and enhance cognitive function in the elderly. In a prior study, it was demonstrated that a diterpene with the 12-deoxyphorbol structure (12-desoxyphorbol 13-isobutyrate: DPB or ER272) stimulated hippocampal neurogenesis in healthy adult mice. This finding suggests that the compound may act as a pharmacological drug that stimulates neurogenesis in mouse models with impaired cognitive function.
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A group of neuroscientists carried out research whose goal was to identify compounds that can be employed in the production of pharmaceuticals to stop the cognitive effects of pathological aging. Using the SAMP8 mouse as a model of pathological aging, the impact of age on hippocampus neurogenesis was investigated. It was demonstrated that episodic and spatial memory in six-month-old SAMP8 mice had been impaired and that the paradigm also resulted in decreased neuroblast and neuronal production and increased astrocyte generation. The chronic administration of ER272 to SAMP8 mice for two months before the onset of cognitive decline enhances cognitive function while concurrently boosting adult hippocampus neurogenesis. The study’s originality comes from the fact that treating SAMP8 mice with TGF-alpha (transforming growth factor alpha) eliminates the abnormalities that were found while also positively affecting neuron formation and cognition. This substance promotes the signaling pathways started by TGF-alpha and facilitates its release both in vivo and in vitro.
Clinical significance
Pharmacological treatments to mitigate the neurological effects of pathological aging may be based on medications that target the release of TGF-alpha. This chemical may function as a pharmacological agent to enhance neurogenesis and cognitive function in the pathologically old brain.
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Conclusion
The process of cerebral aging is complicated and heterogeneous, and it is accompanied by a wide range of chemical alterations. It is vital to continually consider the possible use of novel therapeutic targets in illnesses associated with neurodegeneration and aging.
References
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