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

Genetic linkage analysis of nerve growth factor (beta) in familial Alzheimer's disease.
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家族性阿尔茨海默病神经生长因子(β)的遗传连锁分析。

DOI:
10.1002/ana.410300217
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发表时间:
1991
影响因子:
11.2
通讯作者:
Roses,AD
Roses,AD
中科院分区:
医学1区
文献类型:
--
作者:
Alberts,MJ;Pericak-Vance,MA;Royal,V;Bebout,J;Gaskell,P;Thomas,J;Hung,WY;Clark,C;Earl,N;Roses,AD

文献摘要

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最近的研究没有显示晚发性(平均年龄60岁左右)家族性阿尔茨海默病(FAD)与报道的与早发性FAD相关的21号染色体位点有关联。β -神经生长因子(β - NGF)被认为是FAD发病和治疗的候选基因,其定位于皮质和海马,并能促进胆碱能神经元的生长和存活。β - NGF基因的1.5 kb片段用于检测aBglII限制性片段长度多态性,然后用于连锁分析。共对30个家庭(27个晚发)147名患病成员进行了研究。排除了晚发型FAD与β - NGF的密切关联(θ < 0.03, z < - 2.00)。在不同的尸检证实的家庭中,在受影响的成员之间发现了两个明显的专性交叉。基于这些结果,在所分析的家族中,β - NGF不是导致晚发性FAD的基因。
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 earlyonset 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 aBglII 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.