The bivariate distribution of amyloid-β and tau: relationship with established neurocognitive clinical syndromes
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Summary
Relationship between the bivariate distribution of β-amyloid and tau on PET and established neurocognitive clinical syndromes and abnormal amyloid PET is compatible with normal cognition, highly abnormal tau PET is not.
- Type
- article
- Published
- 2019-09-09
- Cited by
- 179
- References
- 91
- Access
- Open access
- OpenAlex
- https://openalex.org/W2972315303
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:202406432
Keywords
Dementia, Psychology, Alzheimer's disease, Population, Frontotemporal dementia
References
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- Neuropathologic substrate of mild cognitive impairment.
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- Aβ AMYLOID & GLUCOSE METABOLISM IN THREE VARIANTS OF PRIMARY PROGRESSIVE APHASIA
- Mild cognitive impairment as a diagnostic entity
- Amyloid Imaging in Dementias With Atypical Presentation
- Neuropathologically mixed Alzheimer’s and Lewy body disease: burden of pathological protein aggregates differs between clinical phenotypes
- Neurofibrillary tangles but not senile plaques parallel duration and severity of Alzheimer's disease
- Regional variability of imaging biomarkers in autosomal dominant Alzheimer’s disease
Cited by
- Elevated tau PET signal depends on abnormal amyloid levels and is uncommon in unimpaired individuals.
- Amyloid-β-independent regulators of tau pathology in Alzheimer disease
- Staging of tau distribution by positron emission tomography may be useful in clinical staging of Alzheimer disease
- Frontotemporal dementias: main syndromes and underlying brain changes.
- Amyloid-β CSF/PET discordance vs tau load 5 years later: It takes two to tangle
- A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease
- The transformative potential of plasma phosphorylated tau.
- Heavy Tau Burden with Subtle Amyloid β Accumulation in the Cerebral Cortex and Cerebellum in a Case of Familial Alzheimer’s Disease with APP Osaka Mutation
- Longitudinal Cognitive and Biomarker Measurements Support a Unidirectional Pathway in Alzheimer’s Disease Pathophysiology
- Determining Amyloid-β Positivity Using 18F-AZD4694 PET Imaging
- Normalization of CSF pTau measurement by Aβ40 improves its performance as a biomarker of Alzheimer’s disease
- Spatial Relationships between Molecular Pathology and Neurodegeneration in the Alzheimer's Disease Continuum.
- Mechanisms of Pathogenic Tau and Aβ Protein Spreading in Alzheimer’s Disease
- Sensitivity-specificity of tau and Aβ PET in frontotemporal lobar degeneration
- How Can Hearing Loss Cause Dementia?
- Association of amyloid-β CSF/PET discordance and tau load 5 years later
- Variants in PPP2R2B and IGF2BP3 are associated with higher tau deposition
- β-Amyloid and tau biomarkers and clinical phenotype in dementia with Lewy bodies
- Longitudinal anatomic, functional, and molecular characterization of Pick disease phenotypes
- Mesial temporal tau is related to worse cognitive performance and greater neocortical tau load in amyloid-β-negative cognitively normal individuals.
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