Evidence map›Paper›PMID 40766511›Full record

ArticlebioRxiv : the preprint server for biology2025

Amyloid precursor protein dosage normalization rescues neurogenesis and Alzheimer's Disease phenotypes associated with Down Syndrome.

Deepika Patel, Karen Rakowiecki, Orly Lazarov

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Deepika PatelDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA.ORCID 0000-0002-2976-4413
Karen RakowieckiDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA.
Orly LazarovDepartment of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA.

Funding

The role of PS1 in regulation of adult neurogenesis in the intact and Alzheimer?sR01AG033570 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Orly Lazarov · 2009 to 2026
$5.6M
Hippocampal neurogenesis in cognitive function and dysfunction in Alzheimer's disease.R01AG076940 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Orly Lazarov · 2022 to 2026
$3.7M
Plasticity circuits in Alzheimer s diseaseRF1AG033570 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY · 2020 to 2021
$2.9M
Mechanisms underlying sporadic Alzheimer's diseaseR01AG060238 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY · 2018 to 2022
$2.4M
Training program in the biology and translational research on Alzheimer's diseaseand related dementiasT32AG057468 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Stephanie M Cologna, Orly Lazarov · 2017 to 2026
$2.3M
Acceleration of AD Phenotypes in Asymptomatic Mouse ModelsR01AG062251 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY · 2018 to 2022
$2.2M
The role of APP in neurogenesis and AD in Down syndromeRF1AG079002 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY · 2022 to 2022
$2.0M
The role of APP in neurogenesis and AD in Down syndromeR01AG079002 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Orly Lazarov · 2025 to 2026
$1.3M
Signaling pathways regulating hippocampal neurogenesis in the adult mouseR21AG061628 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY · 2019 to 2020
$440k
Connecting Neuronal Hyperexcitability and Sex Differences in Alzheimer's Disease (AD) using biophysically-informed in-silico brain simulations and experimental data from mouse models of ADR21AG087888 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI LAZAROV, ORLY, LEOW, ALEX · 2024 to 2025
$435k
NIA NIH HHS R01 AG033570NIA NIH HHS R01 AG060238NIA NIH HHS R01 AG062251NIA NIH HHS R01 AG076940NIA NIH HHS R01 AG079002NIA NIH HHS R21 AG061628NIA NIH HHS R21 AG087888NIA NIH HHS RF1 AG033570NIA NIH HHS RF1 AG079002NIA NIH HHS T32 AG057468
6 · The paper itself

Abstract

Down Syndrome (DS) is the most abundant genetic form of mental retardation. It is caused by the triplication of partial or complete human chromosome 21 (HSA21). The molecular mechanisms causing it are not fully understood. Previous studies identified "Down syndrome Critical Region" (DSCR) genes that are essential or sufficient for the development of DS. However, these studies are largely inconclusive, due, in part, to the reliance on a small number of epidemiological cases. Amyloid precursor protein (

Indexed as

Alzheimer’s diseaseAmyloid precursor proteinDown SyndromeNeurogenesis

Identifiers

PMID40766511
PMCPMC12324524

What OpenQuestion holds

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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.