Evidence map›Paper›PMID 21068297›Full record

ReviewThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Amyloid-independent mechanisms in Alzheimer's disease pathogenesis.

Sanjay W Pimplikar, Ralph A Nixon, Nikolaos K Robakis, Jie Shen, Li-Huei Tsai

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 3 pooled it
16.7field-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

145 citing papers in PubMed, 3 syntheses or guidelines pooled it, 277 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Smoking and increased Alzheimer's disease risk: a review of potential mechanisms.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014
    Pooled it
  4. Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. In 2024, theFrontiers in aging neuroscience · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

85 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

5 authors at 5 institutions in 1 country.

Sanjay W PimplikarDepartment of Neuroscience, Lerner Research Institute, Cleveland Clinic, and Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, Ohio 44195, USA. pimplis@ccf.org
Ralph A Nixon
Nikolaos K Robakis
Jie Shen
Li-Huei Tsai
Cleveland Clinic Lerner College of Medicine · USHarvard University Press · USHoward Hughes Medical Institute · USIcahn School of Medicine at Mount Sinai · USNew York University · US

Funding

Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
Role of Presenilins in the SynapseR01NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jie Shen · 2001 to 2026
$10.6M
THE ROLE OF Cdk5 IN THE DNA DAMAGE RESPONCE DURING AGING AND NEURODEGENERATIONP01AG027916 · NIA · HARVARD MEDICAL SCHOOL · PI YANKNER, BRUCE A · 2006 to 2010
$7.7M
PS1 &PS2 in Cortical Development and Notch SignalingR01NS042818 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2002 to 2017
$5.7M
STRUCTURE &EXPRESSION OF THE B-PROTEIN-PRECURSOR GENER01AG008200 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI ROBAKIS, NIKOLAOS K · 1988 to 2017
$5.6M
The Cdk5/p35 KinaseR01NS051874 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TSAI, LI-HUEI · 2006 to 2015
$3.7M
PS1 regulates processing and signaling of ephrinB/EphBR37AG017926 · NIA · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI ROBAKIS, NIKOLAOS K · 2005 to 2014
$3.3M
Effects of PS1FAD mutations on PS1-NMDAR association, necroptosis and electrophysiology.RF1AG008200 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ROBAKIS, NIKOLAOS K · 2018 to 2018
$2.8M
Presenilin and APP in the BrainRF1NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2021 to 2021
$2.7M
The In Vivo Role of AICD in Neuronal DysfunctionR01AG026146 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI PIMPLIKAR, SANJAY W · 2006 to 2010
$1.2M
Presenilin1/gamma-secretase regulate the VEGFA/VEGFR2 brain angiogenesis inhibited by FAD mutants.R56AG008200 · NIA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI GEORGAKOPOULOS, ANASTASIOS, ROBAKIS, NIKOLAOS K · 2023 to 2023
$835k
NIA NIH HHS AG008200NIA NIH HHS P01 AG017617NIA NIH HHS P01 AG027916NIA NIH HHS P01-AG027916NIA NIH HHS P01-AG17617NIA NIH HHS R01 AG008200NIA NIH HHS R01 AG026146NIA NIH HHS R01-AG026146NIA NIH HHS R37 AG017926NIA NIH HHS R56 AG008200NIA NIH HHS RF1 AG008200NINDS NIH HHS R01 NS041783NINDS NIH HHS R01-NS041783NINDS NIH HHS R01 NS042818NINDS NIH HHS R01-NS042818NINDS NIH HHS R01 NS051874NINDS NIH HHS R01-NS051874NINDS NIH HHS RF1 NS041783
6 · The paper itself

Abstract

Despite the progress of the past two decades, the cause of Alzheimer's disease (AD) and effective treatments against it remain elusive. The hypothesis that amyloid-β (Aβ) peptides are the primary causative agents of AD retains significant support among researchers. Nonetheless, a growing body of evidence shows that Aβ peptides are unlikely to be the sole factor in AD etiology. Evidence that Aβ/amyloid-independent factors, including the actions of AD-related genes, also contribute significantly to AD pathogenesis was presented in a symposium at the 2010 Annual Meeting of the Society for Neuroscience. Here we summarize the studies showing how amyloid-independent mechanisms cause defective endo-lysosomal trafficking, altered intracellular signaling cascades, or impaired neurotransmitter release and contribute to synaptic dysfunction and/or neurodegeneration, leading to dementia in AD. A view of AD pathogenesis that encompasses both the amyloid-dependent and -independent mechanisms will help fill the gaps in our knowledge and reconcile the findings that cannot be explained solely by the amyloid hypothesis.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansLysosomesNeuronsProtein TransportSignal TransductionAmyloid beta-Peptides

Identifiers

PMID21068297
PMCPMC3426835
OpenAlexW2018494194

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.