E. Almqvist

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Phenotypic characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats.

P S Harper, D Curtis, S. Folstein, 1996, American journal of human genetics.

Contribution of DNA sequence and CAG size to mutation frequencies of intermediate alleles for Huntington disease: evidence from single sperm analyses.

G. van den Engh, D. Sillence, M. Hayden, 1997, Human molecular genetics.

A genome scan for modifiers of age at onset in Huntington disease: The HD MAPS study.

Jane S. Paulsen, J. Mysore, M. MacDonald, 2003, American journal of human genetics.

Molecular analysis of juvenile Huntington disease: the major influence on (CAG)n repeat length is the sex of the affected parent.

F. Squitieri, H. Kremer, M. Anvret, 1993, Human molecular genetics.

The likelihood of being affected with Huntington disease by a particular age, for a specific CAG size.

M. Hayden, R. Brinkman, J. Theilmann, 1997, American journal of human genetics.

Different mechanisms underlie DNA instability in Huntington disease and colorectal cancer.

M. Hayden, S. Thibodeau, D. Tester, 1997, American journal of human genetics.

Predictive testing for persons at risk for homozygosity for CAG expansion in the Huntington disease gene

M. Hayden, F. Squitieri, E. Almqvist, 2003, Clinical genetics.

Ancestral differences in the distribution of the delta 2642 glutamic acid polymorphism is associated with varying CAG repeat lengths on normal chromosomes: insights into the genetic evolution of Huntington disease.

L. Peltonen, I. Kanazawa, M. Anvret, 1995, Human molecular genetics.

Increased instability of intermediate alleles in families with sporadic Huntington disease compared to similar sized intermediate alleles in the general population.

D. Sillence, M. Hayden, J. Buchanan, 1995, Human molecular genetics.

DNA analysis of distinct populations suggests multiple origins for the mutation causing Huntington disease

M. Hayden, M. Anvret, S. Andrew, 1993, Clinical genetics.

Risk reversals in predictive testing for Huntington disease.

M. Hayden, W. Meschino, E. Almqvist, 1997, American journal of human genetics.

Influence of lamotrigine on progression of early Huntington disease

L. Raymond, M. Hayden, C. Jacova, 1999, Neurology.

A worldwide assessment of the frequency of suicide, suicide attempts, or psychiatric hospitalization after predictive testing for Huntington disease.

M. Hayden, D. Craufurd, R. Brinkman, 1999, American journal of human genetics.

Geographical distribution of haplotypes in Swedish families with Huntington's disease

M. Hayden, B. Winblad, P. Goldberg, 1994, Human Genetics.

A Huntington disease-like neurodegenerative disorder maps to chromosome 20p.

M. Hayden, L. Edström, M. Anvret, 1998, American journal of human genetics.

Evidence for a modifier of onset age in Huntington disease linked to the HD gene in 4p16

Jane S. Paulsen, J. Mysore, M. MacDonald, 2004, Neurogenetics.

Sex-dependent mechanisms for expansions and contractions of the CAG repeat on affected Huntington disease chromosomes.

M. Hayden, B. Kremer, Y. P. Goldberg, 1995, American journal of human genetics.

A worldwide study of the Huntington's disease mutation. The sensitivity and specificity of measuring CAG repeats.

Paul W Goldberg, M. Hayden, P. Goldberg, 1994, The New England journal of medicine.

The ‘flap’ endonuclease gene FEN1 is excluded as a candidate gene implicated in the CAG repeat expansion underlying Huntington disease

E. Almqvist, S. Andrew, M. Hayden, 2001, Clinical genetics.

Caudate volume as an outcome measure in clinical trials for Huntington’s disease: a pilot study

L. Raymond, E. Aylward, C. Ross, 2003, Brain Research Bulletin.

Familial influence on age of onset among siblings with Huntington disease.

M. Hayden, C. Ross, R. Brinkman, 2001, American journal of medical genetics.

Low frequency of the APP670/671 mutation in familial Alzheimer's disease in Sweden

B. Winblad, M. Viitanen, L. Lannfelt, 1993, Neuroscience Letters.

At risk for Huntington disease : The PHAROS (Prospective Huntington At Risk Observational Study) cohort enrolled.

E. Almqvist, 2006 .

Measurement of mutational flow implies both a high new-mutation rate for Huntington disease and substantial underascertainment of late-onset cases.

D. Falush, M. Hayden, E. Almqvist, 2001, American journal of human genetics.

Huntington's disease–like 2 (HDL2) in North America and Japan

J. Mysore, M. MacDonald, M. Hayden, 2004, Annals of neurology.

Homozygosity for CAG mutation in Huntington disease is associated with a more severe clinical course.

M. Hayden, D. Rubinsztein, A. Bachoud-Lévi, 2003, Brain : a journal of neurology.

Interaction of normal and expanded CAG repeat sizes influences age at onset of Huntington disease

M. MacDonald, M. Hayden, C. Ross, 2003, American journal of medical genetics. Part A.

Familial aggregation of psychotic symptoms in Huntington's disease.

M. Hayden, T. Bird, D. Tsuang, 2000, The American journal of psychiatry.

Somatic mosaicism in sperm is associated with intergenerational (CAG)n changes in Huntington disease.

B. Kremer, F. Squitieri, E. Almqvist, 1995, Human molecular genetics.

Predictive, pre‐natal and diagnostic genetic testing for Huntington's disease: the experience in Canada from 1987 to 2000

B. Fernandez, M. Hayden, W. Meschino, 2003, Clinical genetics.

Accurate determination of the number of CAG repeats in the Huntington disease gene using a sequence‐specific internal DNA standard

M. Hayden, O. Bruland, Y. P. Goldberg, 1999, Clinical genetics.

Reactions to predictive testing in Huntington disease: case reports of coping with a new genetic status.

B. Winblad, L. Bäckman, M. Anvret, 1997, American journal of medical genetics.

Attitudes towards predictive testing in Huntington's disease--a deep interview study in Sweden.

E. Almqvist, B. Mattsson, 1991, Family practice.