Publications by authors named "Daria Melenteva"
Article Synopsis
- Alzheimer's disease (AD) leads to progressive memory loss, with synaptic loss being a key factor in cognitive decline.
- N-N substituted piperazines, such as the identified compound cmp2, show promise in treating AD due to their ability to cross the blood-brain barrier and activate TRPC6, providing synaptoprotective effects.
- In studies with AD mouse models, cmp2 demonstrated beneficial effects on synaptic plasticity, positioning it as a potential new drug candidate for addressing synaptic deficiencies in the disease.
Alzheimer's disease (AD) is characterized by synaptic dysfunction, which is expressed through the loss of dendritic spines and changes in their morphology. Pharmacological compounds that are able to protect spines in the AD brain are suggested to be novel drugs that would be able to slow down the disease progression. We have recently shown that a positive modulator of transient receptor potential cation channel subfamily C member 6 (TRPC6), the compound N-(2-chlorophenyl)-2-(4-phenylpiperazine-1-yl) acetamide (51164), causes the upregulation of postsynaptic neuronal store-operated calcium entry, maintains mushroom spine percentage, and recovers synaptic plasticity in amyloidogenic mouse models of Alzheimer's disease.
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