ArticleInternational journal of molecular sciences2020
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.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Early diagnosis of Alzheimer's Disease: Graph theoretical analysis of cerebellar network features based on 18F-AV45 PET.PloS one · 2026Article
- Discordant cerebrospinal fluid and positron emission tomography amyloid biomarkers in an APP mutation carrier presenting corticobasal syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Inherited Prion Disease with a 5-octapeptide Repeat Insertion in the PRNP Gene Presenting with Familial Juvenile Dementia.Internal medicine (Tokyo, Japan) · 2025Article
- Article
- Basal forebrain global functional connectivity is preserved in asymptomatic presenilin-1 E280A mutation carriers: Results from the Colombia cohort.The journal of prevention of Alzheimer's disease · 2025Article
- Cerebellum in Alzheimer's disease and other neurodegenerative diseases: an emerging research frontier.MedComm · 2024Review
- Consensus Paper: Cerebellum and Ageing.Cerebellum (London, England) · 2024Review
- International Nuclear Medicine Consensus on the Clinical Use of Amyloid Positron Emission Tomography in Alzheimer's Disease.Phenomics (Cham, Switzerland) · 2023Article
- Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases.International journal of molecular sciences · 2022Article
- Clinical characteristics and genotype-phenotype correlation analysis of familial Alzheimer's disease patients with pathogenic/likely pathogenic amyloid protein precursor mutations.Frontiers in aging neuroscience · 2022Article
- Review
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Authors and funding
13 authors at 3 institutions in 1 country.
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Abstract
We previously identified a novel mutation in amyloid precursor protein from a Japanese pedigree of familial Alzheimer's disease, FAD (Osaka). Our previous positron emission tomography (PET) study revealed that amyloid β (Aβ) accumulation was negligible in two sister cases of this pedigree, indicating a possibility that this mutation induces dementia without forming senile plaques. To further explore the relationship between Aβ, tau and neurodegeneration, we performed tau and Aβ PET imaging in the proband of FAD (Osaka) and in patients with sporadic Alzheimer's disease (SAD) and healthy controls (HCs). The FAD (Osaka) patient showed higher uptake of tau PET tracer in the frontal, lateral temporal, and parietal cortices, posterior cingulate gyrus and precuneus than the HCs (>2.5 SD) and in the lateral temporal and parietal cortices than the SAD patients (>2 SD). Most noticeably, heavy tau tracer accumulation in the cerebellum was found only in the FAD (Osaka) patient. Scatter plot analysis of the two tracers revealed that FAD (Osaka) exhibits a distinguishing pattern with a heavy tau burden and subtle Aβ accumulation in the cerebral cortex and cerebellum. These observations support our hypothesis that Aβ can induce tau accumulation and neuronal degeneration without forming senile plaques.
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