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 (US) |
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Pages (from-to) | 216-219 |
Number of pages | 4 |
Journal | Annals of neurology |
Volume | 30 |
Issue number | 2 |
DOIs | |
State | Published - Aug 1991 |
Externally published | Yes |
ASJC Scopus subject areas
- Neurology
- Clinical Neurology