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Thomas H. Lampe

Researcher at University of Washington

Publications -  23
Citations -  1647

Thomas H. Lampe is an academic researcher from University of Washington. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 16, co-authored 23 publications receiving 1627 citations. Previous affiliations of Thomas H. Lampe include Fred Hutchinson Cancer Research Center & United States Department of Veterans Affairs.

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Absence of linkage of chromosome 21q21 markers to familial Alzheimer's disease

TL;DR: No evidence for linkage was found between familial Alzheimer's disease (FAD) and chromosome 21q21 markers (D 21S1/D21S72 and the amyloid beta gene) and data indicate that FAD is genetically heterogeneous.
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A clinical pathological comparison of three families with frontotemporal dementia and identical mutations in the tau gene (P301L)

TL;DR: These three families demonstrate that a missense mutation in the exon 10 microtubule-binding domain of the tau protein gene can produce severe behavioural abnormalities with frontotemporal lobar atrophy and microscopic tau pathology.
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Phenotypic heterogeneity in familial alzheimer's disease: A study of 24 kindreds

TL;DR: The clinical and neuropathological characteristics occurring in 180 demented individuals from 24 kindreds with familial Alzheimer's disease (FAD) are reported and six findings suggested phenotypic heterogeneity in FAD.
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Familial Alzheimer's disease in American descendants of the Volga Germans: probable genetic founder effect.

TL;DR: Five families are described in which autopsy‐confirmed presenile Alzheimer's disease (AD) has occurred in men and women over multiple generations consistent with autosomal dominant inheritance, and it is likely that the AD in these families represents an autosome dominant gene inherited from one ancestor (the founder effect).
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Myoclonus, seizures, and paratonia in Alzheimer disease.

TL;DR: The incidence of myoclonus, seizures, and paratonia in patients with the clinical diagnosis of probable Alzheimer disease was higher than in most previous studies; the reasons for this finding are discussed.