Evidence map›Paper›PMID 19725915›Full record

ReviewJournal of cellular and molecular medicine2009

Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis.

Pavel F Pavlov, Camilla Hansson Petersen, Elzbieta Glaser, Maria Ankarcrona

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

45 citing papers in PubMed, 79 citations in OpenAlex.

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  10. CoQAntioxidants (Basel, Switzerland) · 2024
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  20. Neurodegenerative Disorders: Spotlight on Sphingolipids.International journal of molecular sciences · 2021
    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

4 authors at 2 institutions in 1 country.

Pavel F PavlovKarolinska Institutet Dainippon Sumitomo Pharma Alzheimer Center, NVS, Novum, Huddinge, Sweden.
Camilla Hansson Petersen
Elzbieta Glaser
Maria Ankarcrona
Karolinska Institutet · SEStockholm University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBrainHumansMitochondriaOrgan SpecificityAmyloid beta-Protein Precursor

Identifiers

PMID19725915
PMCPMC4496119
OpenAlexW2024668613

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.