The Journal of Neurobehavioral Sciences

Yazarlar: Tugce Uzunoglu , Belkis Atasever Arslan

Konular:-

DOI:10.5455/JNBS.1530393578

Anahtar Kelimeler:-

Özet: Alzheimer's disease is a sneaky-onset and progressive neurodegenerative disease characterized by the accumulation of senile plaques formed by amyloid β (Aβ) accumulated in the extracellular environment and intracellular hyperphosphorylated tau proteins characterized by progressive functional disorders and deaths of neurons. Recent studies suggest that the underlying cause of neurodegeneration may be disorders in axonal transport mechanisms. Axonal transport is a dynamic system required for neurons to communicate with each other, to fulfill neuronal functions and to survive. It performs these functions by transporting proteins, organelles, neurotrophic factors and neurotransmitter vesicles throughout the neuron. This system is protected and maintained by a large signal path that contains many proteins. However, by participating in the post-transcriptional regulation of many molecular mechanisms in the body, miRNAs that play a role in many other diseases, such as diseases based on the immune system, cancer and neurodegenerative diseases, can alter the expression of proteins in this signal pathway, leading to tau hyperphosphorylation, impaired axonal transport and hence Alzheimer's disease. In this review study, 12 strains of microRNAs such as miR-133, miR-224, miR-155, miR-34a, miR-125b, miR-9, miR-124, miR29-a/b/c, miR-10b and miR-132 have been investigated for their ability to participate in signaling pathways that play a role in axonal transport and their ability to participate Alzheimer pathology by causing tau hyperphosphorylation.

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