Evidence map›Paper›PMID 20173332›Full record

ArticleNeuro-degenerative diseases2010

Impaired neurotransmitter release in Alzheimer's and Parkinson's diseases.

Jie Shen

Open access · bronzeAbstract read
In one paragraph

Article in Neuro-degenerative diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Impaired dopamine release in Parkinson's disease.Brain : a journal of neurology · 2023
    Review
  4. Article
  5. Article
  6. Experimental and therapeutic medicine · 2021
    Article
  7. Potential therapeutic effects of antagonizing adenosine AMolecular and cellular biochemistry · 2020
    Article
  8. Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  9. Evidence-based complementary and alternative medicine : eCAM · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Function and dysfunction of presenilin.Neuro-degenerative diseases · 2014
    Review
  18. Article
  19. Article
  20. Amyloid-independent mechanisms in Alzheimer's disease pathogenesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Review
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

1 author at 1 institution in 1 country.

Jie ShenCenter for Neurologic Diseases, Brigham and Women's Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, USA. jshen@rics.bwh.harvard.edu
Brigham and Women's Hospital · US

Funding

Role of Presenilins in the SynapseR01NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI Jie Shen · 2001 to 2026
$10.6M
Presenilin and APP in the BrainRF1NS041783 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI SHEN, JIE · 2021 to 2021
$2.7M
NINDS NIH HHS R01 NS041783NINDS NIH HHS RF1 NS041783
6 · The paper itself

Abstract

Mutations in several causative genes have been linked to monogenic forms of Alzheimer's disease (AD) or Parkinson's disease (PD). To look for possible common pathogenic mechanisms underlying age-related neurodegeneration in AD and PD, we employed genetic approaches to investigate systematically the roles of these gene products (e.g. presenilins (PS) for AD; Parkin, DJ-1, PINK1 and LRRK2 for PD) in the mouse brain, especially in neural circuits that are particularly vulnerable in AD or PD. Our series of genetic studies revealed that PS play cell type-specific roles in the developing brain with the most prominent function in the maintenance of neural progenitor cells. In the adult cerebral cortex, where the pathogenesis of AD occurs, loss of PS results in progressive memory impairment and age-related neurodegeneration. Specifically, PS are involved in the regulation of long-term potentiation and NMDA receptor functions. Interestingly, our further genetic dissection in the hippocampal Schaeffer collateral pathway highlighted the importance of presynaptic PS in the activity-dependent regulation of glutamate release and long-term potentiation induction via modulation of calcium release from intracellular stores. Intriguingly, our independent genetic analysis of Parkin, DJ-1, PINK1 and LRRK2 showed a common defect in activity-dependent dopamine release caused by PD-linked mutations in these genes. Together, our genetic studies suggest that presynaptic dysfunction might be a converging early pathogenic event before neurodegeneration in AD and PD.

Indexed as

Alzheimer DiseaseAnimalsHumansMembrane ProteinsMutationNerve Tissue ProteinsNeurotransmitter AgentsParkinson DiseaseMembrane ProteinsNerve Tissue ProteinsNeurotransmitter Agents

Identifiers

PMID20173332
PMCPMC2859234
OpenAlexW2050094059

What OpenQuestion 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 OpenQuestion graph.