Using genetics to enable studies on the prevention of Alzheimer's disease

Crenshaw, D G; Gottschalk, W K; Lutz, M W; Grossman, I; Saunders, A M; Burke, J R; Welsh-Bohmer, K A; Brannan, S K; Burns, D K; Roses, A D

doi:10.1038/clpt.2012.222

Cited by 70Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchGenetic Associations and Epidemiology

Using genetics to enable studies on the prevention of Alzheimer's disease

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Crenshaw, D G, Gottschalk, W K, Lutz, M W, Grossman, I, Saunders, A M, Burke, J R, Welsh-Bohmer, K A, Brannan, S K +2 more·2013·Clinical Pharmacology & Therapeutics

DOI 10.1038/clpt.2012.222PMC PMC4131283

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Abstract

Curing Alzheimer's disease (AD) remains an elusive goal; indeed, it may even prove to be impossible, given the nature of the disease. Although modulating disease progression is an attractive target and will alleviate the burden of the most severe stages, this strategy will not reduce the prevalence of the disease itself. Preventing or (as described in this article) delaying the onset of cognitive impairment and AD will provide the greatest benefit to individuals and society by pushing the onset of disease into the later years of life. Because of the high variability in the age of onset of the disease, AD prevention studies that do not stratify participants by age-dependent disease risk will be operationally challenging, being large in size and of long duration. We present a composite genetic biomarker to stratify disease risk so as to facilitate clinical studies in high-risk populations. In addition, we discuss the rationale for the use of pioglitazone to delay the onset of AD in individuals at high risk.

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The TOMM40 gene, and by extension its protein product, could potentially impact LOAD.
“from a strict association perspective it does appear that the TOMM40 gene, and by extension its protein product, could potentially impact LOAD.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [151]

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Authors: Crenshaw, D. G., Gottschalk, W. K., Lutz, M. W., Grossman, I., Saunders, A. M., Burke, J. R., Welsh-Bohmer, K. A., Brannan, S. K., Burns, D. K., & Roses, A. D.
Affiliations: Duke University (US)
Takeda (United States) (US)
Corresponding author: Roses, A D
ORCID: Gottschalk, W K
Lutz, M W
Saunders, A M
Burke, J R
Welsh-Bohmer, K A
Brannan, S K
Venue: Clinical Pharmacology & Therapeutics
Publisher: Wiley
Published: 2012-11-07
Volume: 93
Issue: 2
Pages: 177-185
ISSN: 0009-9236 (ISSN-L)
1532-6535
DOI: 10.1038/clpt.2012.222
PMC: PMC4131283
OpenAlex: W1988840297
Cited by: 70
References: 67
Citations by year: 2026: 2 · 2025: 2 · 2023: 1 · 2022: 3 · 2021: 6 · 2020: 2 · 2019: 2 · 2018: 5 · 2017: 7 · 2016: 9 · 2015: 10 · 2014: 14 · 2013: 7
FWCI: 6.65
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Clinical Pharmacology & Therapeutics (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (P30AG028377, NIA P30AG-028377)
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 › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
Keywords: Alzheimer's disease, disease prevention, genetic biomarkers, risk stratification, pioglitazone, age of onset, cognitive impairment, vulnerable populations, clinical trial design
MeSH terms: Pioglitazone, Age Factors, Aged, Aged, 80 and over, Alzheimer Disease, Cognition, Humans, Hypoglycemic Agents, Risk Factors, Time Factors, Biomarkers, Randomized Controlled Trials as Topic, Disease Progression, Genetic Predisposition to Disease, Thiazolidinediones

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Using genetics to enable studies on the prevention of Alzheimer's disease

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