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Correcting the MIR‐124/PTPN1 signal abnormality rescues tauopathy in Alzheimer’s disease
Author(s) -
Zhou Yang
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.038498
Subject(s) - tauopathy , hyperphosphorylation , phosphorylation , microbiology and biotechnology , gene silencing , protein phosphatase 2 , phosphatase , biology , neurodegeneration , biochemistry , disease , medicine , gene
Background MicroRNAs have been implicated in diverse physiological and pathological processes. Method Cell Culture and Treatment, RNA Isolation and Quantitative Real‐Time PCR (qRT‐PCR), Preparation of Soluble and Insoluble Fraction. Result We demonstrated that disturbance of the miR‐124/PTPN1 signal induced animbalance of the phosphatase/kinase system by enhancing the tyrosine phosphorylation of GSK‐3β and PP2A, which then caused the activation of GSK‐3β and inactivation of PP2A and ultimately led to AD‐like tauopathy. Conclusion We first replicated the alteration in the miR‐124/PTPN1 signal in AD by artificially upregulating miR‐124 or silencing PTPN1 in the hippocampus of C57 mice and found that disturbance of miR‐124/PTPN1 signal resulted in AD‐like tauopathy, including hyperphosphorylation, aggregation and missorting, as well as learning and memory deficits.