BACKGROUND: A 48 year-old woman presented with an 18 month history of bizarre and complex delusions on a background of social, behavioral and cognitive decline over several years.
Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. The predominant neuropathology is FTLD with TAR DNA-binding protein (TDP-43) inclusions (FTLD-TDP).
OBJECTIVE: We examined the epistatic effect between haplotypes of glycogen synthase kinase-3beta (GSK3B) gene and microtubule-associated protein Tau (MAPT) gene in Alzheimer's disease (AD).
BACKGROUND: Frontotemporal lobar degeneration (FTLD) represents a clinically, pathologically and genetically heterogenous neurodegenerative disorder, often complicated by neurological signs such as mo
Our aim was to characterise PARK2 mutations and clinical features in Hong Kong Chinese with early-onset Parkinson's disease. Subjects were recruited from two major hospitals.
Pedigrees with familial Alzheimer's disease (AD) show considerable phenotypic variability.
Mutations in presenilin-1 (PSEN1) cause autosomal dominant Alzheimer's disease and mutations in MAPT cause the familial tauopathy Frontotemporal dementia linked to chromosome 17 (FTDP-17).
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a combination of motor symptoms.
A family from the south of Western Australia is described with Dutch cerebral amyloid angiopathy (HCHWA-D).
A primary haplotype (H1) of the microtubule-associated protein Tau (MAPT) gene is associated with Parkinson's disease (PD). However, the mechanism for disease susceptibility remains unknown.
The mutation L271V in exon 8 of the presenilin-1 (PS-1) gene was detected in an Alzheimer's disease pedigree.
The majority of cases with frontotemporal dementia (FTD) have no tau deposition in the brain, yet mutations in the tau gene lead to a similar clinical phenotype with insoluble tau depositing in neuro
A variant form of Alzheimer's disease (AD), in which spastic paraparesis (SP) precedes dementia, is characterised by large, noncored, weakly neuritic Abeta-amyloid plaques resembling cotton wool balls
Eleven early-onset dementia families, all with affected individuals who have either presented clinical symptoms of early onset familial Alzheimer's disease (EOFAD) or have been confirmed to have EOFAD
We have identified a large pedigree with clinical symptoms of presenile dementia with motor neuron disease.
Alzheimer's disease and Parkinson's disease are the two common causes of dementia and neurodegeneration.
Both GSK3B and MAPT genes control crucial processes in the cell. We have shown that genetic polymorphisms in these two genes interact to increase risk for late-onset, idiopathic neurodegeneration.
