Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging? DOI Creative Commons

Xinxin Zuo

Aging and Disease, Journal Year: 2025, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2025

Down syndrome (DS), caused by trisomy of chromosome 21 (HSA21), is a complex condition associated with neurodevelopmental impairments and accelerated brain aging, often culminating in early-onset Alzheimer's disease (AD). Central to this aging mitochondrial imbalance, characterized disrupted energy metabolism, increased oxidative stress, impaired dynamics, defective quality control mechanisms like mitophagy. These abnormalities exacerbate neuronal vulnerability, driving cognitive decline neurodegeneration. This review examines the genetic biochemical underpinnings dysfunction DS, focus on role HSA21-encoded genes. We also highlight how dysfunction, amplified stress HSA21 gene dosage effects, converges cellular senescence neuroinflammation accelerate Alzheimer-like pathology DS. Finally, we discuss emerging therapeutic strategies targeting pathways, which hold promise for mitigating neurodegenerative phenotypes improving outcomes

Language: Английский

The potential of natural herbal plants in the treatment and prevention of non-small cell lung cancer: An encounter between ferroptosis and mitophagy DOI
Yujie Yang,

Bing Jiang,

Lijuan Shi

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119555 - 119555

Published: Feb. 1, 2025

Language: Английский

Citations

0

Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging? DOI Creative Commons

Xinxin Zuo

Aging and Disease, Journal Year: 2025, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2025

Down syndrome (DS), caused by trisomy of chromosome 21 (HSA21), is a complex condition associated with neurodevelopmental impairments and accelerated brain aging, often culminating in early-onset Alzheimer's disease (AD). Central to this aging mitochondrial imbalance, characterized disrupted energy metabolism, increased oxidative stress, impaired dynamics, defective quality control mechanisms like mitophagy. These abnormalities exacerbate neuronal vulnerability, driving cognitive decline neurodegeneration. This review examines the genetic biochemical underpinnings dysfunction DS, focus on role HSA21-encoded genes. We also highlight how dysfunction, amplified stress HSA21 gene dosage effects, converges cellular senescence neuroinflammation accelerate Alzheimer-like pathology DS. Finally, we discuss emerging therapeutic strategies targeting pathways, which hold promise for mitigating neurodegenerative phenotypes improving outcomes

Language: Английский

Citations

0