Selected microRNAs Increase Synaptic Resilience to the Damaging Binding of the Alzheimer's Disease Amyloid Beta Oligomers.

ABSTRACT: Alzheimer's disease (AD) is marked by synaptic loss (at early stages) and neuronal death (at late stages). Amyloid beta (Aβ) and tau oligomers can target and disrupt synapses thus driving cognitive decay. Non-demented individuals with Alzheimer's neuropathology (NDAN) are capable of withstanding Aβ and tau toxicity, thus remaining cognitively intact despite presence of AD neuropathology. Understanding the involved mechanism(s) would lead to development of novel effective therapeutic strategies aimed at promoting synaptic resilience to amyloid toxicity. NDAN have a unique hippocampal post-synaptic proteome when compared with AD and control individuals. Potential upstream modulators of such unique proteomic profile are miRNA-485, miRNA-4723 and miRNA-149, which we found differentially expres

SUBMITTER: Zolochevska O 

PROVIDER: S-EPMC7170988 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature