Evidence map›Paper›PMID 28708131›Full record

ReviewNature reviews. Neurology2017

A clinicopathological approach to the diagnosis of dementia.

Fanny M Elahi, Bruce L Miller

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 8 pooled it
15.7field-weighted citation impact, top 1% of its field
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

194 citing papers in PubMed, 8 syntheses or guidelines pooled it, 418 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Trial
  10. Article
  11. Article
  12. Article
  13. Dementia etiology classification using NULISA plasma biomarkers and machine learning.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

134 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Fanny M ElahiMemory and Aging Center, Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, Suite 190, San Francisco, California 94158, USA.
Bruce L MillerMemory and Aging Center, Department of Neurology, University of California, San Francisco, 675 Nelson Rising Lane, Suite 190, San Francisco, California 94158, USA.
University Memory and Aging Center · USUniversity of California, San Francisco · US

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
Multidisciplinary Research Fellowship in Alzheimer’s disease and Related DementiasT32AG023481 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRUCE L MILLER, HOWARD J ROSEN · 2005 to 2026
$7.4M
Effects of chronic inflammation on brain structure and functionR01AG048234 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRAMER, JOEL H · 2015 to 2019
$3.2M
Frontotemporal Dementia Induced Pluripotent Stem Cell ConsortiumR01NS079725 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI GAO, FEN-BIAO, HUANG, YADONG · 2013 to 2016
$3.1M
Multimodal Imaging in Frontotemporal DegenerationK24AG045333 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSEN, HOWARD J · 2013 to 2023
$1.9M
NIA NIH HHS K24 AG045333NIA NIH HHS P01 AG019724NIA NIH HHS P50 AG023501NIA NIH HHS R01 AG048234NIA NIH HHS T32 AG023481NINDS NIH HHS R01 NS079725
6 · The paper itself

Abstract

The most definitive classification systems for dementia are based on the underlying pathology which, in turn, is categorized largely according to the observed accumulation of abnormal protein aggregates in neurons and glia. These aggregates perturb molecular processes, cellular functions and, ultimately, cell survival, with ensuing disruption of large-scale neural networks subserving cognitive, behavioural and sensorimotor functions. The functional domains affected and the evolution of deficits in these domains over time serve as footprints that the clinician can trace back with various levels of certainty to the underlying neuropathology. The process of phenotyping and syndromic classification has substantially improved over decades of careful clinicopathological correlation, and through the discovery of in vivo biomarkers of disease. Here, we present an overview of the salient features of the most common dementia subtypes - Alzheimer disease, vascular dementia, frontotemporal dementia and related syndromes, Lewy body dementias, and prion diseases - with an emphasis on neuropathology, relevant epidemiology, risk factors, and signature signs and symptoms.

Indexed as

Alzheimer DiseaseDementia, VascularFrontotemporal Lobar DegenerationLewy Body DiseasePrion DiseasesHumans

Identifiers

PMID28708131
PMCPMC5771416
OpenAlexW2734680224

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.