Is Alzheimer’s disease a systemic disease?
Open accessAbstract
Although Alzheimer's disease (AD) is the most common neurodegenerative disease, the etiology of AD is not well understood. In some cases, genetic factors explain AD risk, but a high percentage of late-onset AD is unexplained. The fact that AD is associated with a number of physical and systemic manifestations suggests that AD is a multifactorial disease that affects both the CNS and periphery. Interestingly, a common feature of many systemic processes linked to AD is involvement in energy metabolism. The goals of this review are to 1) explore the evidence that peripheral processes contribute to AD risk, 2) explore ways that AD modulates whole-body changes, and 3) discuss the role of genetics, mitochondria, and vascular mechanisms as underlying factors that could mediate both central and peripheral manifestations of AD. Despite efforts to strictly define AD as a homogeneous CNS disease, there may be no single etiologic pathway leading to the syndrome of AD dementia. Rather, the neurodegenerative process may involve some degree of baseline genetic risk that is modified by external risk factors. Continued research into the diverse but related processes linked to AD risk is necessary for successful development of disease-modifying therapies.
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AD is being reframed as a systemic disorder linked to global aging processes rather than a purely localized brain disease.
“Increasingly, AD is being reframed as a systemic disorder linked to global aging processes rather than a purely localized brain disease [4,5].”
From Primary Cilia and Cardiovascular Risk Factors in Alzheimer's Disease (2025) · cites this paper as [4]
The Introduction contrasts the classical view of AD as a primary brain disease with evidence of early systemic manifestations. The Conclusions describe AD as a multifactorial disease affecting both the CNS and the body. The paper does not specifically characterize those shared processes as “global aging processes,” so that part of the claim is not established by this source. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSystemic inflammation is currently beginning to be considered a contributor to AD development.
“In addition, not limited to neuroinflammatory response, systemic inflammation is currently beginning to be considered a contributor to AD development of AD [106, 107].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [106]
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Aerobic capacity and cognitive performance in a cross-sectional aging study
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Alzheimer disease biomarkers are associated with body mass index
Vidoni, E. D., Townley, R. A., Honea, R. A., Burns, J. M., & Initiative, A. D. N. (2011) · Neurology · doi:10.1212/wnl.0b013e318238eec1 · Cited by 140 · see citing works
Self-citationGenetics of Alzheimer's disease: new evidences for an old hypothesis?
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Body mass index in older persons is associated with Alzheimer disease pathology
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Peripheral Mitochondrial Dysfunction in Alzheimer’s Disease: Focus on Lymphocytes
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Mitochondria in Alzheimer's disease
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Peripheral insulin and brain structure in early Alzheimer disease
Burns, J. M., Donnelly, J. E., Anderson, H. S., Mayo, M. S., Spencer-Gardner, L. S., Thomas, G., Cronk, B. B., Haddad, Z., Klima, D., Hansen, D., et al. (2007) · Neurology · doi:10.1212/01.wnl.0000276952.91704.af · Cited by 120 · see citing works
Self-citationBone Density and Brain Atrophy in Early Alzheimer's Disease
Loskutova, N., Honea, R. A., Vidoni, E. D., Brooks, W. M., & Burns, J. M. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1185 · Cited by 118 · see citing works
Self-citationBody Mass Index and Cognitive Decline in Mild Cognitive Impairment
Cronk, B. B., Johnson, D. K., & Burns, J. M. (2010) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e3181a6bf3f · Cited by 109 · see citing works
Self-citationThe Unique Relation of Physical Activity to Executive Function in Older Men and Women
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Cardiorespiratory fitness is associated with atrophy in Alzheimer's and aging over 2 years
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NOX Activity Is Increased in Mild Cognitive Impairment
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Alzheimer's Disease Anti‐Inflammatory Prevention Trial: Design, methods, and baseline results
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Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease
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Self-citationGenome-wide association studies: the key to unlocking neurodegeneration?
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Mitochondria-Targeted Antioxidant Peptides
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Flagged first, then by citations
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Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
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“In addition, not limited to neuroinflammatory response, systemic inflammation is currently beginning to be considered a contributor to AD development of AD [106, 107].”
BackgroundPeripheral and central immune system crosstalk in Alzheimer disease — a research prospectus
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Memantine for the Treatment of Dementia: A Review on its Current and Future Applications
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Phloroglucinol Attenuates the Cognitive Deficits of the 5XFAD Mouse Model of Alzheimer’s Disease
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“Increasingly, AD is being reframed as a systemic disorder linked to global aging processes rather than a purely localized brain disease [4,5].”
- Authors
- Morris, J. K., Honea, R. A., Vidoni, E. D., Swerdlow, R. H., & Burns, J. M.
- Affiliations
- University of Kansas (US)
- Corresponding author
- Burns, Jeffrey M.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2014-09
- Volume
- 1842
- Issue
- 9
- Pages
- 1340-1349
- ISSN
- 0925-4439 (ISSN-L)
- PMC
- PMC4126236
- OpenAlex
- W1966802394
- Cited by
- 219
- References
- 229
- Citations by year
- 2026: 12 · 2025: 12 · 2024: 9 · 2023: 21 · 2022: 21 · 2021: 26 · 2020: 25 · 2019: 20 · 2018: 21 · 2017: 17 · 2016: 16 · 2015: 18 · 2014: 1
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 365 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (F32AG044953, K01AG035042, KL2 TR000119, P30AG035982)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, systemic disease, energy metabolism, genetic risk, mitochondria, vascular mechanisms, multifactorial etiology, disease-modifying therapy, neurodegeneration
- MeSH terms
- Alzheimer Disease, Humans, Risk Factors, Neurodegenerative Diseases
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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