Evidence map›Paper›PMID 34640600›Full record

ReviewJournal of clinical medicine2021

The Clinical and Neuropathological Features of Sporadic (Late-Onset) and Genetic Forms of Alzheimer's Disease.

Tanzil Rujeedawa, Eva Carrillo Félez, Isabel C H Clare, Juan Fortea, Andre Strydom, Anne-Sophie Rebillat, Antonia Coppus, Johannes Levin, Shahid H Zaman

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Tanzil RujeedawaCambridge Intellectual & Developmental Disabilities Research Group, Department of Psychiatry, University of Cambridge, Cambridge CB2 8PQ, UK.
Eva Carrillo FélezCambridge Intellectual & Developmental Disabilities Research Group, Department of Psychiatry, University of Cambridge, Cambridge CB2 8PQ, UK.
Isabel C H ClareCambridge Intellectual & Developmental Disabilities Research Group, Department of Psychiatry, University of Cambridge, Cambridge CB2 8PQ, UK.ORCID 0000-0002-5385-008X
Juan ForteaSant Pau Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Andre StrydomDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE5 8AF, UK.
Anne-Sophie RebillatGeriatrics, Institut Jérôme Lejeune, 75015 Paris, France.ORCID 0000-0003-1995-9177
Antonia CoppusDepartment for Primary and Community Care, Department of Primary and Community Care (149 ELG), Radboud University Nijmegen Medical Center, P.O. Box 9101, 6525 GA Nijmegen, The Netherlands.
Johannes LevinDepartment of Neurology, Ludwig-Maximilians-Universität München, 80539 Munich, Germany.
Shahid H ZamanCambridge Intellectual & Developmental Disabilities Research Group, Department of Psychiatry, University of Cambridge, Cambridge CB2 8PQ, UK.

Funding

Medical Research Council MR/R024901/1Medical Research Council MR/S005145/1Medical Research Council MR/S011277/1
6 · The paper itself

Abstract

The purpose of this review is to compare and highlight the clinical and pathological aspects of genetic versus acquired Alzheimer's disease: Down syndrome-associated Alzheimer's disease in (DSAD) and Autosomal Dominant Alzheimer's disease (ADAD) are compared with the late-onset form of the disease (LOAD). DSAD and ADAD present in a younger population and are more likely to manifest with non-amnestic (such as dysexecutive function features) in the prodromal phase or neurological features (such as seizures and paralysis) especially in ADAD. The very large variety of mutations associated with ADAD explains the wider range of phenotypes. In the LOAD, age-associated comorbidities explain many of the phenotypic differences.

Indexed as

autosomal dominant Alzheimer ’s diseaseclinical featuresdown syndromelate-onset Alzheimer’s diseaseneuropathology

Identifiers

PMID34640600
PMCPMC8509365

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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 Socratic graph.