Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease

Mark J. Alberts, Margaret A. Pericak-Vance, Vernice Royal, Jackie Bebout, Peter Gaskell, John Thomas, Wu Yen Hung, Chris Clark, Nancy Earl, Allen D. Roses

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Recent studies have not shown linkage of late-onset (mean age, >60 years) familial Alzheimer's disease (FAD) to the chromosome 21 locus reported linked to early-onset FAD. Beta nerve growth factor (β-NGF) has been considered a candidate gene in the pathogenesis and therapy of FAD, based on its localization in the cortex and hippocampus and its ability to enhance the growth and survival of cholinergic neurons. A 1.5-kb fragment of the β-NGF gene was used to detect a Bgl II restriction fragment length polymorphism, which was then used for linkage analysis. A total of 30 families (27 late onset) with 147 affected members were studied. Close linkage (θ ≤ 0.03, z ≤ - 2.00) of late-onset FAD with β-NGF was excluded. Two apparent obligate crossovers between affected members were detected in different autopsy-confirmed families. Based on these results, β-NGF is not the gene responsible for late-onset FAD in the families analyzed.

Original languageEnglish (US)
Pages (from-to)216-219
Number of pages4
JournalAnnals of Neurology
Volume30
Issue number2
StatePublished - Aug 1991

Fingerprint

Genetic Linkage
Nerve Growth Factor
Alzheimer Disease
Genes
Chromosomes, Human, Pair 21
Cholinergic Neurons
Aptitude
Age of Onset
Restriction Fragment Length Polymorphisms
Autopsy
Hippocampus
Growth
Alzheimer disease type 2
Therapeutics

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Alberts, M. J., Pericak-Vance, M. A., Royal, V., Bebout, J., Gaskell, P., Thomas, J., ... Roses, A. D. (1991). Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease. Annals of Neurology, 30(2), 216-219.

Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease. / Alberts, Mark J.; Pericak-Vance, Margaret A.; Royal, Vernice; Bebout, Jackie; Gaskell, Peter; Thomas, John; Hung, Wu Yen; Clark, Chris; Earl, Nancy; Roses, Allen D.

In: Annals of Neurology, Vol. 30, No. 2, 08.1991, p. 216-219.

Research output: Contribution to journalArticle

Alberts, MJ, Pericak-Vance, MA, Royal, V, Bebout, J, Gaskell, P, Thomas, J, Hung, WY, Clark, C, Earl, N & Roses, AD 1991, 'Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease', Annals of Neurology, vol. 30, no. 2, pp. 216-219.
Alberts MJ, Pericak-Vance MA, Royal V, Bebout J, Gaskell P, Thomas J et al. Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease. Annals of Neurology. 1991 Aug;30(2):216-219.
Alberts, Mark J. ; Pericak-Vance, Margaret A. ; Royal, Vernice ; Bebout, Jackie ; Gaskell, Peter ; Thomas, John ; Hung, Wu Yen ; Clark, Chris ; Earl, Nancy ; Roses, Allen D. / Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease. In: Annals of Neurology. 1991 ; Vol. 30, No. 2. pp. 216-219.
@article{1f5bd82bb4de4438bee1da1c7d22d307,
title = "Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease",
abstract = "Recent studies have not shown linkage of late-onset (mean age, >60 years) familial Alzheimer's disease (FAD) to the chromosome 21 locus reported linked to early-onset FAD. Beta nerve growth factor (β-NGF) has been considered a candidate gene in the pathogenesis and therapy of FAD, based on its localization in the cortex and hippocampus and its ability to enhance the growth and survival of cholinergic neurons. A 1.5-kb fragment of the β-NGF gene was used to detect a Bgl II restriction fragment length polymorphism, which was then used for linkage analysis. A total of 30 families (27 late onset) with 147 affected members were studied. Close linkage (θ ≤ 0.03, z ≤ - 2.00) of late-onset FAD with β-NGF was excluded. Two apparent obligate crossovers between affected members were detected in different autopsy-confirmed families. Based on these results, β-NGF is not the gene responsible for late-onset FAD in the families analyzed.",
author = "Alberts, {Mark J.} and Pericak-Vance, {Margaret A.} and Vernice Royal and Jackie Bebout and Peter Gaskell and John Thomas and Hung, {Wu Yen} and Chris Clark and Nancy Earl and Roses, {Allen D.}",
year = "1991",
month = "8",
language = "English (US)",
volume = "30",
pages = "216--219",
journal = "Annals of Neurology",
issn = "0364-5134",
publisher = "John Wiley and Sons Inc.",
number = "2",

}

TY - JOUR

T1 - Genetic linkage analysis of nerve growth factor (beta) in familial alzheimer's disease

AU - Alberts, Mark J.

AU - Pericak-Vance, Margaret A.

AU - Royal, Vernice

AU - Bebout, Jackie

AU - Gaskell, Peter

AU - Thomas, John

AU - Hung, Wu Yen

AU - Clark, Chris

AU - Earl, Nancy

AU - Roses, Allen D.

PY - 1991/8

Y1 - 1991/8

N2 - Recent studies have not shown linkage of late-onset (mean age, >60 years) familial Alzheimer's disease (FAD) to the chromosome 21 locus reported linked to early-onset FAD. Beta nerve growth factor (β-NGF) has been considered a candidate gene in the pathogenesis and therapy of FAD, based on its localization in the cortex and hippocampus and its ability to enhance the growth and survival of cholinergic neurons. A 1.5-kb fragment of the β-NGF gene was used to detect a Bgl II restriction fragment length polymorphism, which was then used for linkage analysis. A total of 30 families (27 late onset) with 147 affected members were studied. Close linkage (θ ≤ 0.03, z ≤ - 2.00) of late-onset FAD with β-NGF was excluded. Two apparent obligate crossovers between affected members were detected in different autopsy-confirmed families. Based on these results, β-NGF is not the gene responsible for late-onset FAD in the families analyzed.

AB - Recent studies have not shown linkage of late-onset (mean age, >60 years) familial Alzheimer's disease (FAD) to the chromosome 21 locus reported linked to early-onset FAD. Beta nerve growth factor (β-NGF) has been considered a candidate gene in the pathogenesis and therapy of FAD, based on its localization in the cortex and hippocampus and its ability to enhance the growth and survival of cholinergic neurons. A 1.5-kb fragment of the β-NGF gene was used to detect a Bgl II restriction fragment length polymorphism, which was then used for linkage analysis. A total of 30 families (27 late onset) with 147 affected members were studied. Close linkage (θ ≤ 0.03, z ≤ - 2.00) of late-onset FAD with β-NGF was excluded. Two apparent obligate crossovers between affected members were detected in different autopsy-confirmed families. Based on these results, β-NGF is not the gene responsible for late-onset FAD in the families analyzed.

UR - http://www.scopus.com/inward/record.url?scp=0025813122&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025813122&partnerID=8YFLogxK

M3 - Article

VL - 30

SP - 216

EP - 219

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

IS - 2

ER -