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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
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Published on: February 27, 2018

Establishing bone tissue level changes associated with cognitive impairment.

Ryan D Ross1,2, Bryan Dulion1,2, John Wong1

  • 1Department of Anatomy and Cell Biology, Rush University Medical Center, Chicago, Illinois, United States.

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
|May 22, 2026
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) and osteoporosis share aging links. Bone proteins minichromosomal maintenance protein 3 (MCM3) and ubiquitin carboxyl-terminal hydrolase 24 (USP24) correlate with cognition and Alzheimer's pathology, suggesting cell division processes may link brain and bone aging.

Keywords:
BoneDementiaMinichromosome Maintenance (MCM)ProteomicsUbiquitin Specific Peptidase 24 (USP24)

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Area of Science:

  • Gerontology
  • Neuroscience
  • Bone Biology

Background:

  • Alzheimer's disease (AD) and osteoporosis are prevalent chronic conditions in aging populations.
  • While associations between AD and osteoporosis exist, tissue-level mechanisms remain poorly understood.
  • Investigating bone tissue changes in relation to dementia neuropathology is crucial for understanding aging processes.

Purpose of the Study:

  • To explore bone tissue-level molecular changes associated with Alzheimer's disease (AD) and other dementia neuropathologies.
  • To assess the relationship between bone protein abundance, cognitive function, and neuropathologic markers in aging female participants.
  • To identify potential molecular links between brain aging and bone health.

Main Methods:

  • Unbiased proteomics was performed on thoracic vertebral bone samples from female participants in the ROS and MAP cohorts.
  • Participant cognitive function and clinical characteristics were assessed during study visits.
  • Post-mortem neuropathologic evaluations included beta-amyloid, tau tangles (PHFtau), and other age-related pathologies.
  • Statistical analyses (linear/logistic regression) examined associations between bone protein levels and clinical/neuropathologic data.

Main Results:

  • Bone tissue proteins minichromosomal maintenance protein 3 (MCM3) and ubiquitin carboxyl-terminal hydrolase 24 (USP24) showed positive associations with cognitive function.
  • Increased abundance of MCM3 and USP24 was negatively correlated with paired helical filament tau (PHFtau) tangle density.
  • MCM3 levels were associated with cerebral arteriosclerosis, and USP24 with cerebral amyloid angiopathy.

Conclusions:

  • Bone tissue protein profiles, specifically MCM3 and USP24, are linked to cognitive status and tau pathology in aging women.
  • These findings suggest that mechanisms regulating bone cell division may play a role in the brain-bone aging axis.
  • The observed relationship between brain and bone aging may extend beyond Alzheimer's disease specifically.