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Review
. 2022 Nov 29:14:1006089.
doi: 10.3389/fnagi.2022.1006089. eCollection 2022.

Analysis of shared underlying mechanism in neurodegenerative disease

Rickeem Butler  1 , David Bradford  1 , Kathleen E Rodgers  1
Affiliations
Review

Analysis of shared underlying mechanism in neurodegenerative disease

Rickeem Butler et al. Front Aging Neurosci. .

Abstract

In this review, the relationship between bioenergetics, mitochondrial dysfunction, and inflammation will be and how they contribute to neurodegeneration, specifically in Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS) will be reviewed. Long-term changes in mitochondrial function, autophagy dysfunction, and immune activation are commonalities shared across these age-related disorders. Genetic risk factors for these diseases support an autophagy-immune connection in the underlying pathophysiology. Critical areas of deeper evaluation in these bioenergetic processes may lead to potential therapeutics with efficacy across multiple neurodegenerative diseases.

Keywords: Alzheimer’s disease; amyotrophic lateral sclerosis; bioenergetics; immune; inflammation; metabolic; multiple sclerosis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
AD, MS, and ALS exhibit increased inflammation and bioenergetic changes, ultimately leading to neurodegeneration and furthering disease progression. The cross talk between inflammation and bioenergic dysfunction is dynamic and influences one another, promoting dysregulation. Figure created with BioRender.com .
See this image and copyright information in PMC

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References

    1. 2020 Alzheimer's Association Report (2020). 2020 Alzheimer's disease facts and figures. Alzheimers Dement. 16, 391–460. doi: 10.1002/alz.12068 - DOI - PubMed
    1. Abbott N. J., Patabendige A. A. K., Dolman D. E. M., Yusof S. R., Begley D. J. (2010). Structure and function of the blood–brain barrier. Neurobiol. Dis. 37, 13–25. doi: 10.1016/j.nbd.2009.07.030 - DOI - PubMed
    1. Abel O., Powell J. F., Andersen P. M., Al-Chalabi A. (2012). ALSoD: a user-friendly online bioinformatics tool for amyotrophic lateral sclerosis genetics. Hum. Mutat. 33, 1345–1351. doi: 10.1002/humu.22157, PMID: - DOI - PubMed
    1. Aboul-Enein F., Lassmann H. (2005). Mitochondrial damage and histotoxic hypoxia: a pathway of tissue injury in inflammatory brain disease? Acta Neuropathol. Commun. 109, 49–55. doi: 10.1007/s00401-004-0954-8, PMID: - DOI - PubMed
    1. Adiele R. C., Adiele C. A. (2019). Metabolic defects in multiple sclerosis. Mitochondrion 44, 7–14. doi: 10.1016/j.mito.2017.12.005 - DOI - PubMed