Evidence map›Paper›PMID 19416677›Full record

ReviewExperimental neurology2009

The Alzheimer's disease mitochondrial cascade hypothesis: an update.

Russell H Swerdlow, Shaharyar M Khan

Abstract readReview
In one paragraph

Review in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing 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

112 citing papers in PubMed.

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52 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

2 authors.

Russell H SwerdlowDepartment of Neurology, University of Kansas School of Medicine, Kansas City, USA. rswerdlow@kumc.edu
Shaharyar M Khan

Funding

Cytochrome Oxidase Polymorphisms in AgingR01AG022407 · NIA · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI SWERDLOW, RUSSELL H · 2005 to 2007
$446k
NIA NIH HHS R01 AG022407
6 · The paper itself

Abstract

In 2004 we proposed the mitochondrial cascade hypothesis of sporadic Alzheimer's disease (AD). Our hypothesis assumed sporadic and autosomal dominant AD are not etiologically homogeneous, considered evidence that AD pathology is not brain-limited, and incorporated aging theory. The mitochondrial cascade hypothesis asserted: (1) inheritance determines mitochondrial baseline function and durability; (2) mitochondrial durability influences how mitochondria change with age; and (3) when mitochondrial change reaches a threshold, AD histopathology and symptoms ensue. We now review the reasoning used to formulate the hypothesis, discuss pertinent interim data, and update its tenants. Readers are invited to consider the conceptual strengths and weaknesses of this hypothesis.

Indexed as

AgingAlzheimer DiseaseAmyloidosisAnimalsBrainCell CycleHumansMitochondriaRisk Factorstau Proteinstau Proteins

Identifiers

PMID19416677
PMCPMC2710413

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.