Evidence map›Paper›PMID 38513771›Full record

ReviewAgeing research reviews2024

Alzheimer's drugs, APPlication for Down syndrome?

Deborah K Sokol, Debomoy K Lahiri

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. The striatum is an early, accurate indicator of amyloid burden using [Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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.

Deborah K SokolDepartment of Neurology, Section Pediatrics, Indiana University of Medicine, Riley Hospital, 575 Riley Hospital Drive, Indianapolis, IN 46202, USA.
Debomoy K LahiriDepartment of Psychiatry, 320 West 15th St, Indianapolis, IN 46202, USA; Department of Medical and Molecular Genetics, 320 West 15th St, Indianapolis, IN 46202, USA; Stark Neurosciences Research Institute, 320 West 15th St, Indianapolis, IN 46202, USA; Indiana Alzheimer's Disease Research Center, 320 West 15th St, Indianapolis, IN 46202, USA. Electronic address: dlahiri@iupui.edu.
Indiana University · USIndiana University Health · US

Funding

TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI MUFSON, ELLIOTT JAY · 1997 to 2024
$39.7M
Research Education ComponentP30AG010133 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SAYKIN, ANDREW J · 1991 to 2020
$37.3M
Research Education ComponentP30AG072976 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI ANDREW J SAYKIN · 2021 to 2026
$24.1M
Role of microRNA in regulating Fe, Amyloid, and Tau (FeAT) in Alzheimer's diseaseR56AG072810 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2021 to 2021
$630k
Neurobiological Role of MicroRNA in Alzheimer'sR56AG051086 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2023 to 2023
$627k
Brain protein alteration by vascular overexpressed miRNA (BravomiR)R21AG076202 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2022 to 2022
$435k
Testing a Novel Approach to Solve the On-target, Off-site Effects of Alzheimer's DrugsR21AG056007 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2019 to 2020
$435k
Alzheimer's disease-linked microRNA Exploration of UTR Polymorphisms (AdmiRE-UP)R21AG074539 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2022 to 2022
$435k
NIA NIH HHS P01 AG014449NIA NIH HHS P30 AG010133NIA NIH HHS P30 AG072976NIA NIH HHS R21 AG056007NIA NIH HHS R21 AG074539NIA NIH HHS R21 AG076202NIA NIH HHS R56 AG051086NIA NIH HHS R56 AG072810
6 · The paper itself

Abstract

Accumulation of the amyloid β (Aβ) peptide, derived from Aβ precursor protein (APP), is a trait of Down syndrome (DS), as is early development of dementia that resembles Alzheimer's disease (AD). Treatments for this AD in DS simply do not. New drug therapies for AD, e.g., Lecanemab, are monoclonal antibodies designed to clear amyloid plaques composed of Aβ. The increasingly real ability to target and dispose of Aβ favors the use of these drugs in individuals with AD in DS, and, perhaps as earlier intervention for cognitive impairment. We present pertinent similarities between DS and AD in adult DS subjects, discuss challenges to target APP metabolites, and suggest that recently developed antibody treatments against Aβ may be worth investigating to treat AD in DS.

Indexed as

Alzheimer DiseaseDown SyndromeAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAntibodies, MonoclonalHumansPhenotypeAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAntibodies, MonoclonalAgingAmyloidDownDYRK1Trisomy 21

Identifiers

PMID38513771
PMCPMC11903029
OpenAlexW4392946612

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.