Oxidative and nitrosative stress are widely recognized as critical factors in the pathogenesis and progression of Alzheimer disease (AD) and its earlier stage, amnestic mild cognitive impairment (MCI). A major source of free radicals that lead to oxidative and nitrosative damage is mitochondria. This review paper discusses oxidative and nitrosative stress and markers thereof in the brain, along with redox proteomics, which are techniques that have been pioneered in the Butterfield laboratory. Selected biological alterations in and oxidative and nitrosative modifications of mitochondria in AD and MCI and systems of relevance thereof also are presented. The review article concludes with a section on the implications of mitochondrial oxidative and nitrosative stress in MCI and AD with respect to imaging studies in and targeted therapies toward these disorders. Taken together, this review provides support for the notion that brain mitochondrial alterations in AD and MCI are key components of oxidative and nitrosative stress observed in these two disorders, and as such, they provide potentially promising therapeutic targets to slow and hopefully one day stop the progression of AD, which is a devastating dementing disorder.
|Number of pages||22|
|State||Published - Sep 2020|
Bibliographical noteFunding Information:
Funding: This work was funded in part by a grant from the National Institutes of Health [R01AG060056] (D.A.B.). The APC was funded by the same grant.
© 2020 by the authors. Licensee MDPI, Basel, Switzerland.
- Alzheimer disease and mild cognitive impairment
- Amyloid beta-peptide
- Mitochondrial dysfunction
- Oxidative and nitrosative stress
- Redox proteomics
ASJC Scopus subject areas
- Molecular Biology
- Clinical Biochemistry
- Cell Biology