Evidence map›Paper›PMID 37667136›Full record

ReviewNature medicine2023

Emerging diagnostics and therapeutics for Alzheimer disease.

Wade K Self, David M Holtzman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed, 5 pooled it
64.3field-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

176 citing papers in PubMed, 5 syntheses or guidelines pooled it, 338 citations in OpenAlex.

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  4. Clinical criteria for limbic-predominant age-related TDP-43 encephalopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Pooled it
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116 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 1 institution in 1 country.

Wade K SelfDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA.ORCID http://orcid.org/0000-0003-1648-6124
David M HoltzmanDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO, USA. holtzman@wustl.edu.ORCID http://orcid.org/0000-0002-3400-0856
Hope Center for Neurological Disorders · US

Funding

Project 4 (Genetic modifiers for APOE-associated Alzheimer's disease pathogenesis)U19AG069701 · NIA · MAYO CLINIC JACKSONVILLE · PI ALISON M GOATE · 2021 to 2026
$42.0M
Effect of APOE on CNS Neurons: Role of LRPRF1NS090934 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2020 to 2025
$6.5M
Novel Strategies and Mechanisms to Target APOE and Alzheimer's DiseaseRF1AG047644 · NIA · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M., HYMAN, BRADLEY T. · 2019 to 2019
$3.8M
NIA NIH HHS RF1 AG047644NIA NIH HHS U19 AG069701NINDS NIH HHS RF1 NS090934
6 · The paper itself

Abstract

Alzheimer disease (AD) is the most common contributor to dementia in the world, but strategies that slow or prevent its clinical progression have largely remained elusive, until recently. This Review highlights the latest advances in biomarker technologies and therapeutic development to improve AD diagnosis and treatment. We review recent results that enable pathological staging of AD with neuroimaging and fluid-based biomarkers, with a particular emphasis on the role of amyloid, tau and neuroinflammation in disease pathogenesis. We discuss the lessons learned from randomized controlled trials, including some supporting the proposal that certain anti-amyloid antibodies slow cognitive decline during the mildly symptomatic phase of AD. In addition, we highlight evidence for newly identified therapeutic targets that may be able to modify AD pathogenesis and progression. Collectively, these recent discoveries-and the research directions that they open-have the potential to move AD clinical care toward disease-modifying treatment strategies with maximal benefits for patients.

Indexed as

Alzheimer DiseaseCognitive DysfunctionHumansNeuroimagingTechnology

Identifiers

PMID37667136
OpenAlexW4386437808

What Socratic holds

Textmetadata
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.