Evidence map›Paper›PMID 39832071›Full record

ReviewBiogerontology2025

The potential link between the development of Alzheimer's disease and osteoporosis.

Fariha Nasme, Jyotirmaya Behera, Prisha Tyagi, Nabendu Debnath, Jeff C Falcone, Neetu Tyagi

Abstract readReview
In one paragraph

Review in Biogerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Fariha NasmeDepartment of Physiology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Jyotirmaya BeheraDivision of Immunology, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA.
Prisha TyagiDepartment of Physiology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Nabendu DebnathCentre for Molecular Biology, Central University of Jammu, Rahya-Suchani (Bagla) Samba, Jammu, Jammu & Kashmir, 181143, India.
Jeff C FalconeDepartment of Physiology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA.
Neetu TyagiDepartment of Physiology, School of Medicine, University of Louisville, Louisville, KY, 40202, USA. neetu.tyagi@louisville.edu.

Funding

American Heart Association 24TPA1304527American Heart Association TPA-971566American Heart Association-American Stroke Association 24TPA1304527American Heart Association-American Stroke Association 971566
6 · The paper itself

Abstract

Alzheimer's disease (AD) and osteoporosis (OP) pose distinct but interconnected health challenges, both significantly impacting the aging population. AD, a neurodegenerative disorder characterized by memory impairment and cognitive decline, is primarily associated with the accumulation of abnormally folded amyloid beta (Aβ) peptides and neurofibrillary tangles in the brain. OP, a skeletal disorder marked by low bone mineral density, involves dysregulation of bone remodeling and is associated with an increased risk of fractures. Recent studies have revealed an intriguing link between AD and OP, highlighting shared pathological features indicative of common regulatory pathophysiological pathways. In this article, we elucidate the signaling mechanisms that regulate the pathology of AD and OP and offer insights into the intricate network of factors contributing to these conditions. We also examine the role of bone-derived factors in the progression of AD, underscoring the plausibility of bidirectional communication between the brain and the skeletal system. The presence of amyloid plaques in the brain of individuals with AD is akin to the accumulation of brain Aβ in vascular dementia, pointing towards the need for further investigation of shared molecular mechanisms. Moreover, we discuss the role of bone-derived microRNAs that may regulate the pathological progression of AD, providing a novel perspective on the role of skeletal factors in neurodegenerative diseases. The insights presented here should help researchers engaged in exploring innovative therapeutic approaches targeting both neurodegenerative and skeletal disorders in aging populations.

Indexed as

Alzheimer DiseaseOsteoporosisAmyloid beta-PeptidesAnimalsBone RemodelingBrainHumansAmyloid beta-PeptidesAging populationAmyloid beta (Aβ)Bone-derived factorsBone mineral densityBone remodelingNeurodegenerative disordersVascular dementia

Identifiers

PMID39832071
PMCPMC12087362

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.