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1.
Journal of Zhejiang University. Medical sciences ; (6): 485-498, 2023.
Artigo em Inglês | WPRIM | ID: wpr-1009910

RESUMO

Alzheimer's disease (AD) is a multifactorial and heterogenic disorder. MiRNA is a class of non-coding RNAs with 19-22 nucleotides in length that can regulate the expression of target genes in the post-transcriptional level. It has been found that the miRNAome in AD patients is significantly altered in brain tissues, cerebrospinal fluid and blood circulation, as compared to healthy subjects. Experimental studies have suggested that expression changes in miRNA could drive AD onset and development via different mechanisms. Therefore, targeting miRNA expression to regulate the key genes involved in AD progression is anticipated to be a promising approach for AD prevention and treatment. Rodent AD models have demonstrated that targeting miRNAs could block biogenesis and toxicity of amyloid β, inhibit the production and hyper-phosphorylation of τ protein, prevent neuronal apoptosis and promote neurogenesis, maintain neural synaptic and calcium homeostasis, as well as mitigate neuroinflammation mediated by microglia. In addition, animal and human studies support the view that miRNAs are critical players contributing to the beneficial effects of cell therapy and lifestyle intervention to AD. This article reviews the most recent advances in the roles, mechanisms and applications of targeting miRNA in AD prevention and treatment based on rodent AD models and human intervention studies. The potential opportunities and challenges in clinical application of targeting miRNA for AD patients are also discussed.


Assuntos
Animais , Humanos , MicroRNAs/genética , Doença de Alzheimer/prevenção & controle , Peptídeos beta-Amiloides , Apoptose , Microglia
2.
Progress in Biochemistry and Biophysics ; (12)2006.
Artigo em Chinês | WPRIM | ID: wpr-594209

RESUMO

It is well believed that learning and memory is one of the functions of sleep.Not only does the sleep after learning aid memory consolidation, but enough sleep before learning is necessary for memory formation.Due to the net increase in synaptic strength, waking plasticity has a cost in terms of energy requirements, space requirements, and progressively saturates the capacity to learning.The review will focus on the role of sleep which is to downscale synaptic strength to a baseline level that is beneficial for learning and memory.

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