Evidence map›Paper›PMID 23327526›Full record

ReviewAnnual review of medicine2013

Toward the treatment and prevention of Alzheimer's disease: rational strategies and recent progress.

Sam Gandy, Steven T DeKosky

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
9.9field-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

57 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Therapeutic effects of a novel synthetic α-secretase.Frontiers in aging neuroscience · 2024
    Article
  6. Article
  7. Article
  8. Review
  9. Neuroprotective effects of donepezil against AβEuropean journal of medical research · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Liver Growth Factor "LGF" as a Therapeutic Agent for Alzheimer's Disease.International journal of molecular sciences · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. A Novel Nanosystem Realizing Curcumin Delivery Based on FeFrontiers in bioengineering and biotechnology · 2020
    Article
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.

Sam GandyMount Sinai School of Medicine and James J. Peters Veterans Affairs Medical Center, New York, New York 10029, USA. samuel.gandy@mssm.edu
Steven T DeKosky
Icahn School of Medicine at Mount Sinai · USUniversity of Virginia · US

Funding

RECRUITMENT COREU19AG010483 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDMAN, HOWARD · 2013 to 2020
$80.6M
Vascular Moderators of the Impact of Alzheimer's Pathology in the Young-OldP01AG025204 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Milos D Ikonomovic · 2005 to 2026
$56.5M
TREATMENT OF DEPRESSION IN ALZHEIMER'S DISEASEP50AG005133 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECKER, JAMES T. · 1985 to 2019
$43.0M
VESICULAR LOCALIZATION AND FUNCTION OF PRESENILIN 1 FRAGMENTP50AG005138 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI SCHIMMING, CORBETT · 1985 to 2019
$37.9M
Model for SorCS1-mediated Diabetes with DementiaR01NS075685 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GANDY, SAMUEL E. · 2012 to 2015
$1.5M
Alzheimer Mouse Model for Intraneuronal Amyloid-Beta Oligomer BiologyI01BX000348 · VA · JAMES J PETERS VA MEDICAL CENTER · PI GANDY, SAMUEL E. · 2009 to 2012
–
BLRD VA I01 BX000348NIA NIH HHS AG025204NIA NIH HHS AG05133NIA NIH HHS P01 AG025204NIA NIH HHS P50 AG005133NIA NIH HHS P50 AG005138NIA NIH HHS P50 AG05138NIA NIH HHS U19 AG010483NINDS NIH HHS R01 NS075685
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the major cause of late-life brain failure. In the past 25 years, autosomal dominant forms of AD were found to be primariy attributable to mutations in one of two presenilins, polytopic proteins that contain the catalytic site of the γ-secretase protease that releases the amyloid beta (Aβ) peptide. Some familial AD is also due to mutations in the amyloid precursor protein (APP), but recently a mutation in APP was discovered that reduces Aβ generation and is protective against AD, further implicating amyloid metabolism. Prion-like seeding of amyloid fibrils and neurofibrillary tangles has been invoked to explain the stereotypical spread of AD within the brain. Treatment trials with anti-Aβ antibodies have shown target engagement, if not significant treatment effects. Attention is increasingly focused on presymptomatic intervention, because Aβ mismetabolism begins up to 25 years before symptoms begin. AD trials deriving from new biological information involve extraordinary international collaboration and may hold the best hope for success in the fight against AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesMutationAmyloid beta-Protein PrecursorBrainDNAGlobal HealthHumansImmunologic FactorsIncidencePractice Guidelines as TopicAmyloid beta-PeptidesAmyloid beta-Protein PrecursorDNAImmunologic Factors

Identifiers

PMID23327526
PMCPMC3625402
OpenAlexW2135220503

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.