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MicroRNAs as diagnostic and therapeutic tools for Alzheimer’s disease: advances and limitations

Journal Article · · Neural Regeneration Research
 [1];  [2]
  1. Univ. of California, Merced, CA, (United States). Dept. of Molecular & Cellular Biology; St. Georges Univ. School of Medicine, Grenada. Dept. of Medicine; Los Alamos National Lab, Los Alamos, NM, (United States). Dept. of Physics and Engineering; University Otago, New Zealand
  2. Univ. of Otago, Dunedin, New Zealand. Dept. of Anatomy
Alzheimer’s disease (AD) is the most common age-related, progressive neurodegenerative disease. It is characterized by memory loss and cognitive decline and responsible for most cases of dementia in the elderly. Late-onset or sporadic AD accounts for > 95% of cases, with age at onset > 65 years. Currently there are no drugs or other therapeutic agents available to prevent or delay the progression of AD. The cellular and molecular changes occurring in the brains of individuals with AD include accumulation of β-amyloid peptide and hyperphosphorylated tau protein, decrease of acetylcholine neurotransmitter, inflammation, and oxidative stress. Aggregation of β-amyloid peptide in extracellular plaques and the hyperphosphorylated tau protein in intracellular neurofibrillary tangles are characteristic of AD. A major challenge is identifying molecular biomarkers of the early-stage AD in patients as most studies have been performed with blood or brain tissue samples (postmortem) at late-stage AD. Subjects with mild cognitive impairment almost always have the neuropathologic features of AD with about 50% of mild cognitive impairment patients progressing to AD. They could provide important information about AD pathomechanism and potentially also highlight minimally or noninvasive, easy-to-access biomarkers. MicroRNAs are dysregulated in AD, and may facilitate the early detection of the disease and potentially the continual monitoring of disease progression and allow therapeutic interventions to be evaluated. Four recent reviews have been published of microRNAs in AD, each of which identified areas of weakness or limitations in the reported studies. Importantly, studies in the last three years have shown considerable progress in overcoming some of these limitations and identifying specific microRNAs as biomarkers for AD and mild cognitive impairment. Further large-scale human studies are warranted with less disparity in the study populations, and using an appropriate method to validate the findings.
Research Organization:
Los Alamos National Lab. (LANL), Los Alamos, NM (United States)
Sponsoring Organization:
USDOE
Grant/Contract Number:
AC52-06NA25396
OSTI ID:
1628699
Journal Information:
Neural Regeneration Research, Journal Name: Neural Regeneration Research Journal Issue: 2 Vol. 14; ISSN 1673-5374
Publisher:
Chinese Association of Rehabilitation Medicine (CARM)Copyright Statement
Country of Publication:
United States
Language:
English

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Cited By (7)

Long Noncoding RNA NEAT1 Aggravates Aβ-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease journal January 2019
MicroRNA-Mediated Control of Inflammation and Tolerance in Pregnancy journal April 2019
Cofilin 2 in Serum as a Novel Biomarker for Alzheimer’s Disease in Han Chinese journal August 2019
Neuroinflammation as a Common Feature of Neurodegenerative Disorders journal September 2019
Risk Factors Associated with Mild Cognitive Impairment аmong Apparently Healthy People and the Role of MicroRNAs journal October 2019
Cerebral Amyloid Angiopathy, Alzheimer’s Disease and MicroRNA: miRNA as Diagnostic Biomarkers and Potential Therapeutic Targets journal October 2019
MicroRNAs in Alzheimer’s Disease: Diagnostic Markers or Therapeutic Agents? journal June 2019

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