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Ageing as a risk factor for neurodegenerative disease
Abstract
Ageing is the primary risk factor for most neurodegenerative diseases, including Alzheimer disease (AD) and Parkinson disease (PD). One in ten individuals aged ≥65 years has AD and its prevalence continues to increase with increasing age. Few or no effective treatments are available for ageing-related neurodegenerative diseases, which tend to progress in an irreversible manner and are associated with large socioeconomic and personal costs. This Review discusses the pathogenesis of AD, PD and other neurodegenerative diseases, and describes their associations with the nine biological hallmarks of ageing: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, deregulated nutrient sensing, stem cell exhaustion and altered intercellular communication. The central biological mechanisms of ageing and their potential as targets of novel therapies for neurodegenerative diseases are also discussed, with potential therapies including NAD+ precursors, mitophagy inducers and inhibitors of cellular senescence.
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“The use of primary human monocytes also has several advantages: (i) their human origin enables the study of human-specific disease phenotypes and molecular mechanisms, (ii) monocytes derived from patients with AD may contain cell-intrinsic properties specific to that patient, and (iii) monocytes derived from patients with AD and age-matched controls may exhibit age-relevant phenotypes, given that”
From Understanding monocyte-driven neuroinflammation in Alzheimer’s disease using human cortical organoid microphysiological systems (2025) · cites this paper as [75]
In the citing paper
“Aging, which remains the largest risk factor for LOAD, is associated with low-grade systemic inflammation (termed “inflammaging”) [20, 21].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [21]
In the citing paper
“Age‐related alterations in the brain microenvironment gradually led to increased BBB permeability and leakiness, neuronal degeneration, production of reactive oxygen species (ROS) and inflammation. 54 , 55 , 56”
From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [54]
In the citing paper
“Aging is known to be the primary driver of many neurodegenerative diseases, including Alzheimer’s disease (AD) [53].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [53]
In the citing paper
“This concurrence could explain the strong link between increased age and ND [83].”
From Untangling senescent and damage‐associated microglia in the aging and diseased brain (2023) · cites this paper as [83]
In the citing paper
“Aging is the predominant risk factor for cognitive dysfunction (Kalache and Gatti, 2003; Partridge et al., 2018) and several neurodegenerative disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD) (Hou et al., 2019; López-Otín et al., 2013; Niccoli et al., 2017).”
From Atlas of the aging mouse brain reveals white matter as vulnerable foci (2023) · cites this paper as Hou et al., 2019
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RETRACTED ARTICLE: Parkin and PINK1 mitigate STING-induced inflammation
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Metadata
- Authors
- Hou, Y., Dan, X., Babbar, M., Wei, Y., Hasselbalch, S. G., Croteau, D. L., & Bohr, V. A.
- Affiliations
- National Institute on Aging (US)
- University of Copenhagen (DK)
- Corresponding author
- Bohr, Vilhelm A.
- ORCID
- Venue
- Nature Reviews Neurology
- Published
- 2019-09-09
- Volume
- 15
- Issue
- 10
- Pages
- 565-581
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- OpenAlex
- W2972368830
- Semantic Scholar
- 4f2aec225c7ce5314a73bd30acc5348f6086766b
- Cited by
- 3,310
- References
- 209
- Citations by year
- 2026: 441 · 2025: 639 · 2024: 675 · 2023: 534 · 2022: 474 · 2021: 359 · 2020: 178 · 2019: 8
- FWCI
- 22.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- National Institute on Aging
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- aging, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease, genomic instability, telomere shortening, epigenetic modifications, proteostasis, mitochondrial dysfunction, cellular senescence, nutrient sensing, stem cell exhaustion, intercellular communication, NAD+ precursors, mitophagy, senolytics, therapeutic target
- MeSH terms
- Aging, Brain, DNA Damage, Humans, Risk Factors, Neurodegenerative Diseases, Epigenesis, Genetic, Mitophagy
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