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Peer-reviewedCC BYFrontiers in aging neuroscience

Deciphering the effects of aging on Alzheimer's disease based on mitochondrial dysfunction and neuroinflammation.

  • Yamei Luo1
  • Haoli Yu1
  • Jun Zhang1
  • Zhihong Wu2
  • Haiyan Zhang3
  1. 1School of Medical Technology, Chongqing Three Gorges Medical College, Chongqing, China.
  2. 2School of Public Health and Management, Chongqing Three Gorges Medical College, Chongqing, China.
  3. 3School of Traditional Chinese Medicine, Chongqing Three Gorges Medical College, Chongqing, China.
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Abstract

Alzheimer's disease (AD), a neurological disorder characterized by progressive deterioration of cognitive function, has complex pathogenic mechanisms and lacks curative therapies with proven efficacy. Aging and inflammatory responses, which play indispensable roles in the onset and progression of AD, are closely intertwined with mitochondrial dysfunction. During aging, a series of degenerative alterations, including accumulated mitochondrial DNA (mtDNA) mutations, excessive mitochondrial reactive oxygen species (ROS) accumulation, disrupted mitochondrial quality control (MQC) and disturbed energy metabolism, further induce structural mitochondrial damage. This damage causes the leakage of damage-associated molecular patterns (DAMPs) and activates numerous downstream inflammatory signaling pathways. In brain tissue, inflammatory cytokines, which continuously facilitate blood-brain barrier (BBB) disruption, aberrant activation of microglial cells, tau protein hyperphosphorylation, as well as Aβ accumulation, drive an endlessly amplified neuroinflammatory cascade that leads to irreversible neuronal damage and fuels the initiation and progression of AD. In this review, we clarify the regulatory effects of aging on AD pathogenesis through the mitochondrial dysfunction-chronic inflammation axis and ultimately focus on mitochondrial-targeted therapies, with future outlooks for AD treatment provided.

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Cite

BibTeXRIS
BibTeX
@article{luo2026deciphering,
  title = {{Deciphering the effects of aging on Alzheimer's disease based on mitochondrial dysfunction and neuroinflammation.}},
  author = {Yamei Luo and Haoli Yu and Jun Zhang and Zhihong Wu and Haiyan Zhang},
  journal = {Frontiers in aging neuroscience},
  year = {2026},
  month = oct,
  doi = {10.3389/fnagi.2026.1991837},
  url = {https://europepmc.org/article/MED/43011645},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Deciphering the effects of aging on Alzheimer's disease based on mitochondrial dysfunction and neuroinflammation.
AU  - Yamei Luo
AU  - Haoli Yu
AU  - Jun Zhang
AU  - Zhihong Wu
AU  - Haiyan Zhang
PY  - 2026
DA  - 2026/10/27
JO  - Frontiers in aging neuroscience
DO  - 10.3389/fnagi.2026.1991837
UR  - https://europepmc.org/article/MED/43011645
AB  - Alzheimer's disease (AD), a neurological disorder characterized by progressive deterioration of cognitive function, has complex pathogenic mechanisms and lacks curative therapies with proven efficacy. Aging and inflammatory responses, which play indispensable roles in the onset and progression of AD, are closely intertwined with mitochondrial dysfunction. During aging, a series of degenerative alterations, including accumulated mitochondrial DNA (mtDNA) mutations, excessive mitochondrial reactive oxygen species (ROS) accumulation, disrupted mitochondrial quality control (MQC) and disturbed energy metabolism, further induce structural mitochondrial damage. This damage causes the leakage of damage-associated molecular patterns (DAMPs) and activates numerous downstream inflammatory signaling pathways. In brain tissue, inflammatory cytokines, which continuously facilitate blood-brain barrier (BBB) disruption, aberrant activation of microglial cells, tau protein hyperphosphorylation, as well as Aβ accumulation, drive an endlessly amplified neuroinflammatory cascade that leads to irreversible neuronal damage and fuels the initiation and progression of AD. In this review, we clarify the regulatory effects of aging on AD pathogenesis through the mitochondrial dysfunction-chronic inflammation axis and ultimately focus on mitochondrial-targeted therapies, with future outlooks for AD treatment provided.
SN  - 1663-4365
ER  -