Current knowledge of chromosome 12 susceptibility genes for late-onset Alzheimer's disease

D’Introno, Alessia; Solfrizzi, Vincenzo; Colacicco, Anna Maria; Capurso, Cristiano; Amodio, Margherita; Todarello, Orlando; Capurso, Antonio; Kehoe, Patrick G.; Panza, Francesco

doi:10.1016/j.neurobiolaging.2005.09.020

Cited by 23Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchGenetic Associations and Epidemiology

Current knowledge of chromosome 12 susceptibility genes for late-onset Alzheimer's disease

D’Introno, Alessia, Solfrizzi, Vincenzo, Colacicco, Anna Maria, Capurso, Cristiano, Amodio, Margherita, Todarello, Orlando, Capurso, Antonio, Kehoe, Patrick G. +1 more·2006·Neurobiology of Aging

DOI 10.1016/j.neurobiolaging.2005.09.020

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Abstract

In the last decade, it has become more apparent the important role genes play in the development of late-onset Alzheimer's disease (AD). Great efforts, involving human genome scans and candidate gene studies, have been given towards identifying susceptibility genes for AD. A number of regions on different chromosomes have been reported to demonstrate linkage for AD. Of these, findings on chromosome 12 are some of the most compelling. Worldwide genetic association studies pre-dating and subsequent to recent linkage studies have identified and focused upon a number of genes that map to the areas of reported linkage on chromosome 12, however, analyses of those genes studied to date, on the whole, remain inconclusive and ambiguous. This paper reviews studies that have provided evidence of linkage for AD on chromosome 12 and in turn discusses the work conducted to date on candidate genes that have been identified and map to the chromosome 12 regions of interest.

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Telomere shortening may be accelerated by oxidative insults, inflammatory elements, excessive stress, and other risk factors related to AD onset.
“Telomere shortening may be accelerated by oxidative insults, inflammatory elements, excessive stress, and many other risk factors related to the AD onset [505].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [505]

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Authors: D’Introno, A., Solfrizzi, V., Colacicco, A. M., Capurso, C., Amodio, M., Todarello, O., Capurso, A., Kehoe, P. G., & Panza, F.
Affiliations: University of Bari Aldo Moro (IT)
University of Foggia (IT)
University of Bristol (GB)
Corresponding author: Panza, Francesco
ORCID: D’Introno, Alessia
Solfrizzi, Vincenzo
Capurso, Cristiano
Capurso, Antonio
Kehoe, Patrick G.
Panza, Francesco
Venue: Neurobiology of Aging
Publisher: Elsevier BV
Published: 2006-11
Volume: 27
Issue: 11
Pages: 1537-1553
ISSN: 0197-4580 (ISSN-L)
DOI: 10.1016/j.neurobiolaging.2005.09.020
OpenAlex: W1984068399
Cited by: 23
References: 156
Citations by year: 2020: 1 · 2019: 2 · 2018: 1 · 2016: 1 · 2015: 2 · 2013: 1 · 2012: 3
FWCI: 0.29
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Aging (publishedVersion)
PubMed (publishedVersion)
Explore Bristol Research (publishedVersion)
Bristol Research (University of Bristol) (submittedVersion)
CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
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: late-onset Alzheimer's disease, chromosome 12, susceptibility genes, genetic linkage, candidate genes, genetic association studies
MeSH terms: Alzheimer Disease, Chromosome Mapping, Chromosomes, Human, Pair 12, DNA-Binding Proteins, Humans, Receptors, LDL, Transcription Factors, Linkage Disequilibrium, Telomere, Genetic Predisposition to Disease, Low Density Lipoprotein Receptor-Related Protein-1

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Current knowledge of chromosome 12 susceptibility genes for late-onset Alzheimer's disease

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