Neural Regeneration Research ›› 2023, Vol. 18 ›› Issue (2): 319-.doi: 10.4103/1673-5374.346472

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Turning up the NAD+-mitophagy axis to treat Alzheimer’s disease

Evandro F. Fang*, Alexander Anisimov   

  1. Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, Lørenskog, Norway (Fang EF, Anisimov A)
    The Norwegian Centre on Healthy Ageing (NO-Age), Oslo, Norway (Fang EF)
  • Online:2023-02-15 Published:2022-08-06
  • Contact: Evandro F. Fang, PhD, e.f.fang@medisin.uio.no.
  • Supported by:
    This work was supported by National Natural Science Foundation of China (No. 81971327), Akershus University Hospital (Nos. 269901, 261973), the Civitan Norges Forskningsfond for Alzheimers sykdom (No. 281931), the Czech Republic-Norway KAPPA programme (with Martin Vyhnálek, No. TO01000215), and the Rosa sløyfe/Norwegian Cancer Society & Norwegian Breast Cancer Society (No. 207819) to EFF.

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Abstract: The increase in the prevalence of individuals with Alzheimer’s disease (AD) combined with the lack of a cure calls for the development of novel therapies against AD (Canter et al., 2016). The key disease-defining pathological features of AD are the accumulation of extracellular amyloid-beta (Aβ) plaques (accompanied by increasing intracellular Aβ1–42) and higher intracellular neurofibrillary tangles, comprised mostly of hyperphosphorylated tau protein/pTau (Goedert, 2015; Hardy, 2017). It is evident that the elderly are more predisposed to develop AD, and thus aging is considered to be the primary risk factor for AD. By extrapolation, strategies that delay aging may also slow down (if not stop) AD.