Clinical and Pathological Characteristics of Frontotemporal Lobar Degeneration(FTLD) and Molecular Genetics of Tau Protein.
- Author:
Sung Il WOO
1
Author Information
1. Department of Neuropsychiatry, Soonchunhyang University Hospital, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Tau;
FTLD;
PiD;
PSP;
CBD;
FTDP-17
- MeSH:
Amyloid;
Dementia;
Frontotemporal Dementia;
Frontotemporal Lobar Degeneration;
Molecular Biology*;
Neurofibrillary Tangles;
Parkinsonian Disorders;
Pathology;
Pick Disease of the Brain;
Plaque, Amyloid;
Prednisolone;
Supranuclear Palsy, Progressive;
tau Proteins*;
Tauopathies
- From:Journal of the Korean Society of Biological Psychiatry
2003;10(2):97-106
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Criticisms about amyloid cascade hypothesis of Alzheimer's disease(AD) are based on the findings, first, that the degree of dementia does not correlate with the number of plaques, and second, that the neurofibrillary tangle formation seems to predate plaque formation. In addition, neurofibrillary tangle counts correlate well with the degree of cognitive impairment. These findings suggest the independent importance of tau abnormality in AD research which is involved in the neurofibrillary tangle formation. Recently, tau pathology without amyloid deposits and mutations in tau protein gene were reported to be the major pathogenic mechanism in Pick's disease, progressive supranuclear palsy, corticobasal degeneration and FTDP-17(frontotemporal dementia and parkinsonism linked with chromosome 17). These data suggest that understanding the causes and consequences of tau dysfunction might give new clinical and therapeutic solutions to many known tauopathies.
