The Role of the MAPK Signaling Pathway in LTP Reduction Associated with Alzheimer’s Disease
DOI:
https://doi.org/10.47611/jsrhs.v14i1.8544Keywords:
MAPK, Alzheimer's Disease, LTP, long-term potentationAbstract
The MAPK signaling pathway plays a key role in contributing to a major symptom of Alzheimer’s Disease: memory loss. Memory power can be measured by LTP (long-term potentiation) levels, as LTP is the process that strengthens synapses, allowing them to store memories upon repeated stimulation. The primary mechanism behind the MAPK signaling pathway is a large phosphorylation cascade between several proteins, including Ras, Raf, MEK, ERK, NF-kB, and other cytoplasmic and nuclear proteins. Under normal circumstances, the MAPK pathway results in an increase in LTP by boosting glutamate receptor concentration on a postsynaptic neuron. However, the overstimulation of this pathway results in excitotoxicity, causing cytoskeletal collapse and neuronal death, a phenomenon that commonly occurs due to Alzheimer’s Disease. Treatments for Alzheimer’s Disease can target stages of the MAPK signal transduction pathway or change the expression of genes that cause excitotoxicity. Understanding the MAPK signaling pathway is crucial for the development of memory improving Alzheimer’s treatments, remedies that would greatly better the lives of Alzheimer’s patients.
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