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Familial Risk for Alzheimer Disease in Ethnic Minorities

Familial Risk for Alzheimer Disease in Ethnic Minorities EDITORIAL Familial Risk for Alzheimer Disease in Ethnic Minorities Nondiscriminating Genes PIDEMIOLOGICAL AND molecular evidence tional levels resulting in more tenuous ties with the health suggests that there are multiple etiologies care system, less access to tertiary health care facilities, for Alzheimer disease (AD). Studies of the problems in transportation to clinics, lack of informa- incidence and patterns of transmission in tion about AD, lack of information about help that may E families demonstrate that relatives of af- be available through involvement with a center, and lack fected individuals have an increased risk of developing of culturally or racially compatible professional staff at AD compared with members of the general population. the local sites. For example, the results of a survey of With the exception of rare (probably ,1%) cases har- the sites involved in minority recruitment for CERAD boring pathogenic mutations in the amyloid precursor (Consortium to Establish a Registry for Alzheimer Dis- protein or presenilin genes, susceptibility is governed by ease) emphasized the importance of familiarity, person- a complex interaction of genes and environmental fac- to-person contact, and relationships of trust. They also tors. The most potent factor identified to date is the e4 noted that connection http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Neurology American Medical Association

Familial Risk for Alzheimer Disease in Ethnic Minorities

JAMA Neurology , Volume 57 (1) – Jan 1, 2000

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Publisher
American Medical Association
Copyright
Copyright 2000 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6149
eISSN
2168-6157
DOI
10.1001/archneur.57.1.28
Publisher site
See Article on Publisher Site

Abstract

EDITORIAL Familial Risk for Alzheimer Disease in Ethnic Minorities Nondiscriminating Genes PIDEMIOLOGICAL AND molecular evidence tional levels resulting in more tenuous ties with the health suggests that there are multiple etiologies care system, less access to tertiary health care facilities, for Alzheimer disease (AD). Studies of the problems in transportation to clinics, lack of informa- incidence and patterns of transmission in tion about AD, lack of information about help that may E families demonstrate that relatives of af- be available through involvement with a center, and lack fected individuals have an increased risk of developing of culturally or racially compatible professional staff at AD compared with members of the general population. the local sites. For example, the results of a survey of With the exception of rare (probably ,1%) cases har- the sites involved in minority recruitment for CERAD boring pathogenic mutations in the amyloid precursor (Consortium to Establish a Registry for Alzheimer Dis- protein or presenilin genes, susceptibility is governed by ease) emphasized the importance of familiarity, person- a complex interaction of genes and environmental fac- to-person contact, and relationships of trust. They also tors. The most potent factor identified to date is the e4 noted that connection

Journal

JAMA NeurologyAmerican Medical Association

Published: Jan 1, 2000

References