of the genes are downregulated. In that regard, AD therapeutics focused on antagomiR-mediated silencing of"upregulated"microRNAs (miRs) may be more feasible since upregulated miRs in AD continue to increase with the disease progression, as opposed to agomiR-mediated overexpression of down-regulated miRs with unpredictable reduced presence and relative short-life of 1-3h under pathological conditions in AD brain. Studies reported thus far indicate that most of the upregulated pathogenic genes in AD are regulated by pro-inflammatory microRNAs (miRs). Given the precedence of chronic neuroinflammation in triggering AD-like neurodegeneration and multifactorial nature of AD, silencing inflammation-specific micro-RNAs using antisense-microRNAs may be an effective adjuvant therapeutic strategy to prevent, halt or cure AD.
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Neelima B. Chauhan (2020) studied this question.
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