Mechanistic complexities of bone loss in Alzheimer’s disease: a review
Abstract
Purpose/Aim : Alzheimer's disease (AD), the primary cause of dementia in the elderly, is one of the leading age-related neurodegenerative diseases worldwide. While AD is notorious for destroying memory and cognition, dementia patients also experience greater incidence of bone loss and skeletal fracture than age-matched neurotypical individuals, greatly impacting their quality of life. Despite the significance of this comorbidity, there is no solid understanding of the mechanisms driving early bone loss in AD. Here, we review studies that have evaluated many of the obvious risk factors shared by dementia and osteoporosis, and illuminate emerging work investigating covert pathophysiological mechanisms shared between the disorders that may have potential as new risk biomarkers or therapeutic targets in AD. Conclusions : Skeletal deficits emerge very early in clinical Alzheimer's progression, and cannot be explained by coincident factors such as aging, female sex, mobility status, falls, or genetics. While research in this area is still in its infancy, studies implicate several potential mechanisms in disrupting skeletal homeostasis that include direct effects of amyloid-beta pathology on bone cells, neurofibrillary tau-induced damage to neural centers regulating skeletal remodeling, and/or systemic Wnt/Beta-catenin signaling deficits. Data from an increasing number of studies substantiate a role for the newly discovered "exercise hormone" irisin and its protein precursor FNDC5 i…
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Patients with osteoporosis often have a higher incidence of AD.
“Patients with osteoporosis often have a higher incidence of AD, and bone loss is frequently detected early in the progression of AD, preceding substantial cognitive decline25–27.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [25]
Bone loss is frequently detected early in the progression of AD, preceding substantial cognitive decline.
“Patients with osteoporosis often have a higher incidence of AD, and bone loss is frequently detected early in the progression of AD, preceding substantial cognitive decline25–27.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [25]
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- Authors
- Frame, G., Bretland, K. A., & Dengler-Crish, C. M.
- Affiliations
- Kent State University (US)
- Northeast Ohio Medical University (US)
- Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, OH, USA
- ORCID
- Frame, Gabrielle
- Venue
- Connective Tissue Research
- Publisher
- Informa UK Limited
- Published
- 2019-06-11
- Volume
- 61
- Issue
- 1
- Pages
- 4-18
- ISSN
- 0300-8207 (ISSN-L)
- 1607-8438
- OpenAlex
- W2949519242
- Cited by
- 44
- References
- 0
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 10 · 2023: 5 · 2022: 2 · 2021: 8 · 2020: 4 · 2019: 1
- FWCI
- 0.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Connective Tissue Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, bone loss, osteoporosis, dementia, skeletal homeostasis, amyloid-beta, tau pathology, Wnt/β-catenin signaling, irisin, FNDC5, exercise hormones, fracture risk, biomarkers, therapeutic target
- MeSH terms
- Aging, Alzheimer Disease, Fibronectins, Humans, Osteoporosis, Biomarkers, Wnt Signaling Pathway
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