Frontotemporal dementia: Genotypes, phenotypes and more problems to be solved

Neurobiology of Aging

Volumn 22, Issue 1, 2001, Pages 113-114

  Bird, Thomas D ^a  

^a UNIVERSITY OF WASHINGTON   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMYLOID BETA PROTEIN; TAU PROTEIN;

ALZHEIMER DISEASE; BRAIN REGION; CLINICAL FEATURE; DISEASE CLASSIFICATION; DISEASE PREDISPOSITION; FAMILY HISTORY; FRONTOTEMPORAL DEMENTIA; GENE MUTATION; GENOTYPE; HUMAN; NERVE CELL; NEUROFIBRILLARY TANGLE; NEUROPATHOLOGY; NONHUMAN; NOTE; ONSET AGE; PHENOTYPE; PRIORITY JOURNAL;

ALZHEIMER DISEASE; DEMENTIA; GENOTYPE; HUMANS; MICROTUBULE-ASSOCIATED PROTEINS; MUTATION; PHENOTYPE; TAU PROTEINS;

EID: 0035054732     PISSN: 01974580     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0197-4580(00)00197-4     Document Type: Note

References (9)

1. A clinical pathological comparison of three families with frontotemporal dementia and identical mutations in the tau gene (P301L)
2. Impaired social response reversal: A case of 'acquired sociopathy'
3. Focal and asymmetric cortical degeneration syndromes
4. A family with autosomal dominant, non-Alzheimer's presenile dementia
5. Missense and silent tau gene mutations cause frontotemporal dementia with parkinsonism-chromosome 17 type, by affecting multiple alternative RNA splicing regulatory elements
6. Frequency of tau mutations in three series of non-Alzheimer's degenerative dementia
7. Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex
8. Emergence of artistic talent in frontotemporal dementia
9. The frequency of tau gene mutations in familial and sporadic cases of non-Alzheimer dementia