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 language | English |
|---|---|
| Pages (from-to) | 216-219 |
| Number of pages | 4 |
| Journal | Annals of Neurology |
| Volume | 30 |
| Issue number | 2 |
| State | Published - Aug 1 1991 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
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, 01.08.1991, p. 216-219.Research output: Contribution to journal › Article
}
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 - 1991/8/1
Y1 - 1991/8/1
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.
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M3 - Article
C2 - 1680304
AN - SCOPUS:0025813122
VL - 30
SP - 216
EP - 219
JO - Annals of Neurology
JF - Annals of Neurology
SN - 0364-5134
IS - 2
ER -