Spermidine Drosten CAS 124-20-9

The synaptic plasticity of neurons is the ability of the nervous system to change the structure and function of synapses in order to adapt to changes in the external environment, which can be divided into structural plasticity and functional plasticity [8-9]. Long-term potentiation (LTP) is one of the main manifestations of synaptic plasticity. A large number of studies have confirmed that the synaptic plasticity of neurons is closely related to learning and memory, and most researchers believe that the cellular basis for learning and memory is LTP [10]. Therefore, regulating synaptic plasticity, especially increasing LTP, is an important way to improve learning and memory. There are a large number of N-methyl-D-aspartate (NMDA) receptors on synapses, which are involved in the regulation of synaptic plasticity in the central nervous system, especially for LTP adjustment. It has been reported that the activation of NMDA receptors can promote the influx of calcium ions and generate LTP, thereby achieving the purpose of improving learning and memory.

Studies have confirmed that the reduction of Spermidine Droste levels in the brain impairs the specific spatial learning and related memory abilities of rats in the water maze test [14]. The systemic administration and injection of spermidine into the amygdala significantly improved the mice’s performance in inhibitory avoidance behavior, fear episodic memory, and social recognition tasks, and facilitated and re-consolidated fear memory. Varun et al. found that memory impairment caused by the expansion of the presynaptic active area (AZ area) with increasing age. After Drosophila was fed spermidine (30dSpd), the core scaffold proteins in the AZ area such as Bruchpilot (BRP) and RIM-binding Protein (RBP) and other expressions no longer increase, and the AZ region no longer expands with age, thereby inhibiting age-related memory impairment [19-20]. This indicates that spermidine has the ability to improve learning and memory, and this ability may be achieved by regulating synaptic plasticity.

There are oxidative systems and antioxidant systems in the body, and under normal circumstances, the two are in a state of dynamic balance. When the body is subjected to various harmful stimuli, excess polymer active substances such as oxygen free radicals and lipid peroxides are produced in the body, and the oxidative capacity exceeds the antioxidant capacity, breaking the balance between oxidation and anti-oxidation, resulting in oxidative stress. , causing cell and tissue damage. After the brain tissue of the body is damaged, a strong oxidative stress response may occur, a large number of oxygen free radicals will accumulate, and neurons will be damaged.

Autophagy is a self-protection mechanism of cells, and the main role of this process is to degrade defective organelles and misfolded proteins in cells. In neuronal cells, autophagy plays an extremely important role in maintaining the stability of the intracellular environment [34]. Basal levels of autophagy have been reported to have protective effects on neural cells.