ReviewDevelopmental neurobiology2019
Neuropathological correlates of amyloid PET imaging in Down syndrome.
Review in Developmental neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
34 citing papers in PubMed, 49 citations in OpenAlex.
- Measurement of Tau Protein and Aβ Amyloid Plaques in Postmortem Human Brains of Down Syndrome and Alzheimer's Disease by Using [Synapse (New York, N.Y.) · 2026Article
- Measurement of tau protein and Aβ amyloid plaques in postmortem human brains of Down syndrome and Alzheimer's disease by using [bioRxiv : the preprint server for biology · 2026Article
- Joint spatial associations of amyloid beta and tau pathology in Down syndrome and preclinical Alzheimer's disease: Cross-sectional associations with early cognitive impairments.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Cargo of small extracellular vesicles from neuronal origin shows progression of dementia in individuals with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The striatum is an early, accurate indicator of amyloid burden using [Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Exploring peripheral fluid biomarkers for early detection of Alzheimer's disease in Down syndrome: A literature review.Heliyon · 2025Review
- A comparison of multiple amyloid PET radiotracers for Down syndrome clinical trials.Brain communications · 2025Article
- Down Syndrome Biobank Consortium: A perspective.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Reduced synaptic proteins and SNARE complexes in Down syndrome with Alzheimer's disease and the Dp16 mouse Down syndrome model: Impact of APP gene dose.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Vesicular Glutamate Transporter Changes in the Cortical Default Mode Network During the Clinical and Pathological Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Radiomics Analysis of Brain [Diagnostics (Basel, Switzerland) · 2022Article
- Cell models for Down syndrome-Alzheimer's disease research.Neuronal signaling · 2022Review
- Joint-label fusion brain atlases for dementia research in Down syndrome.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Cortical atrophy and amyloid and tau deposition in Down syndrome: A longitudinal study.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Emergence of distinct and heterogeneous strains of amyloid beta with advanced Alzheimer's disease pathology in Down syndrome.Acta neuropathologica communications · 2021Article
- The Clinical and Neuropathological Features of Sporadic (Late-Onset) and Genetic Forms of Alzheimer's Disease.Journal of clinical medicine · 2021Review
- Deciphering the links between psychological stress, depression, and neurocognitive decline in patients with Down syndrome.Neurobiology of stress · 2021Review
- Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Down syndrome (DS) results in an overproduction of amyloid-β (Aβ) peptide associated with early onset of Alzheimer's disease (AD). DS cases have Aβ deposits detectable histologically as young as 12-30 years of age, primarily in the form of diffuse plaques, the type of early amyloid pathology also seen at pre-clinical (i.e., pathological aging) and prodromal stages of sporadic late onset AD. In DS subjects aged >40 years, levels of cortical Aβ deposition are similar to those observed in late onset AD and in addition to diffuse plaques involve cored plaques associated with dystrophic neurites (neuritic plaques), which are of neuropathological diagnostic significance in AD. The purpose of this review is to summarize and discuss findings from amyloid PET imaging studies of DS in reference to postmortem amyloid-based neuropathology. PET neuroimaging applied to subjects with DS has the potential to (a) track the natural progression of brain pathology, including the earliest stages of amyloid accumulation, and (b) determine whether amyloid PET biomarkers predict the onset of dementia. In addition, the question that is still incompletely understood and relevant to both applications is the ability of amyloid PET to detect Aβ deposits in their earliest form.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.