Publications by authors named "N G Zernov"
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.
The transient receptor potential cation channel, subfamily C, member 6 (TRPC6), has been believed to adjust the formation of an excitatory synapse. The positive regulation of TRPC6 engenders synapse enlargement and improved learning and memory in animal models. TRPC6 is involved in different synaptoprotective signaling pathways, including antagonism of N-methyl-D-aspartate receptor (NMDAR), activation of brain-derived neurotrophic factor (BDNF) and postsynaptic store-operated calcium entry.
View Article and Find Full Text PDFSynapse loss in the brain of Alzheimer's disease patients correlates with cognitive dysfunctions. Drugs that limit synaptic loss are promising pharmacological agents. The transient receptor potential cation channel, subfamily C, member 6 (TRPC6) regulates the formation of an excitatory synapse.
View Article and Find Full Text PDFAlzheimer'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.
View Article and Find Full Text PDFCalcium/calmodulin-dependent protein kinase II (CaMKII) and neuronal store-operated calcium entry (nSOCE) have been implicated in the development of Alzheimer's disease (AD). nSOCE is involved in regulation of dendritic spine shape, particularly in stability of mushroom spines that play role in formation of strong synapses. CaMKII is involved in regulation of induction of long-term potentiation, that is needed for shaping of memory.
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