Genetic linkage studies in Alzheimer's disease families
References (38)
- et al.
A new probe for the diagnosis of myotonic muscular dystrophy
Science
(1987) - et al.
Evidence for linkage of CMT neuropathy to the Duffy locus on chromosome 1
Am. J. Hum. Genet.
(1982) - et al.
Genetic linkage evidence for heterogeneity in CMT neuropathy (HMSN Type I)
Ann. Neurol.
(1983) Estimating the power of a proposed linkage study: A practical computer simulation approach
Am. J. Hum. Genet.
(1986)- et al.
Familial Alzheimer's dementia: A prevalent disorder with specific clinical features
Psychol. Med.
(1984) - et al.
Familial aggregation in Alzheimer's disease: Comparison of risk among relatives of early-and-late-onset cases, and among male and female relatives in successive generations
Neurology
(1988) - et al.
- et al.
- et al.
Neuro-ophthalmologic findings in vestibulocerebellar ataxia
Arch. Neurol.
(1986) - et al.
Neuropsychologic features of early and late onset Alzheimer's disease
Arch. Neurol.
(1986)
Is Alzheimer's disease inherited: A methologic review
Integr. Psychiatr.
Clinical and genetic investigation in autosomal dominant limb-girdle muscular dystrophy
Neurology
Linkage of autosomal dominant type I hereditary motor and sensory neuropathy to the Duffy locus on chromosome 1
J. Neurol. Neurosurg. Psych.
Analysis of Huntington disease linkage and age-of-onset distributions
Genet. Epid. Suppl.
Alzheimer's disease: A study of epidemiologic aspects
Ann. Neurol.
Age-of-onset correction available for linkage analysis (LIPED)
Am. J. Hum. Genet.
Senile demenita: A clinical sociomedical and genetic study
Acta. Psychiat. Scand.
Easy calculations of lod scores and genetic risks on small computers
Am. J. Hum. Genet.
Cited by (131)
Genetics of Alzheimer Disease
2013, Emery and Rimoin's Principles and Practice of Medical GeneticsAdmixture analysis of age at first suicide attempt
2009, Journal of Psychiatric ResearchCitation Excerpt :Age at onset (AAO) has frequently been used as a key indicator in strategies of this type. For example, differences in AAO have been used to identify specific susceptibility factors for Alzheimer’s disease and Duchenne–Becker muscular dystrophy (Koenig et al., 1989; Pericak-Vance et al., 1988). Similar approaches have generated interesting results in several adult psychiatric populations with bipolar disorder, schizophrenia and obsessive compulsive disorder (Bellivier et al., 2001; Delorme et al., 2005; Schurhoff et al., 2004).
Genetics of Alzheimer's Disease: A Centennial Review
2007, Neurologic ClinicsCitation Excerpt :Although the exact steps involved in the cascade of events in this pathophysiologic mechanism are as yet unknown and debatable, this mechanism has clearly set the stage for the ongoing drug discovery efforts for AD [84–86]. The failure of multiple research groups to replicate the initial linkage reports to chromosome 21 [35] in various independent collections of AD families led to the hypothesis that AD may be a heterogeneous disorder [39,40,87]. In 1991, Pericak-Vance and colleagues [88] reported the results of a genome search they conducted in EOAD and LOAD families, whereby they found linkage to chromosome 21 in their EOAD families, and a novel locus on chromosome 19.
Admixture analysis of age at onset in schizophrenia
2004, Schizophrenia ResearchMaking drug discovery a SN(i)P
2000, Drug Discovery Today
- 2
R. J. Bartlett is a recipient of an ADRDA/Allied Signal Faculty Scholar Award.
- 1
The authors thank Drs. J. F. Gusella and G. D. Stewart for providing the DNA probes D21S1/D21S11 and D21S16; Drs. Michael Boehnke and R. C. Elston for their helpful comments; Wendy Smith, Fiona Francis, James Koh, Edward Hanson, Kenneth M. Wilkinson, and Sharon Musick for expert assistance with the polymorphism and DNA analysis; Peggy Pate and Helen Harbett for technical assistance with the family data analysis; Laurita Melton and Penny Ligon for manuscript preparation. This work was supported by the Joseph and Kathleen Bryan Alzheimer's Disease Research Center (AG05128), by NS19999 and NS23008 from the NINCDS, by a grant from the Denver Foundation for Health and Research, and by Clinical Research Unit M01-RR-30 from the NIGMS.