Evidence map›Paper›PMID 25114088›Full record

ReviewJournal of Alzheimer's disease : JAD2015

Common mechanisms of Alzheimer's disease and ischemic stroke: the role of protein kinase C in the progression of age-related neurodegeneration.

Brandon P Lucke-Wold, Ryan C Turner, Aric F Logsdon, James W Simpkins, Daniel L Alkon, Kelly E Smith, Yi-Wen Chen, Zhenjun Tan, Jason D Huber, Charles L Rosen

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Brandon P Lucke-WoldDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV, USA The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
Ryan C TurnerDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV, USA The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
Aric F LogsdonThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV, USA.
James W SimpkinsThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
Daniel L AlkonBlanchette Rockefeller Neurosciences Institute, Morgantown, WV, USA.
Kelly E SmithThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV, USA.
Yi-Wen ChenThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
Zhenjun TanDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV, USA The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
Jason D HuberThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV, USA.
Charles L RosenDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV, USA The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV, USA.
West Virginia University · USBlanchette Rockefeller Neurosciences Institute · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Sally Lynn Hodder · 2012 to 2026
$81.0M
ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
Research Training Program in the Behavioral and Biomedical SciencesT32GM081741 · NIGMS · WEST VIRGINIA UNIVERSITY · PI BERREBI, ALBERT S, SIMPKINS, JAMES W. · 2008 to 2018
$2.1M
NIA NIH HHS P01 AG027956NIGMS NIH HHS T32 GM081741NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Ischemic stroke and Alzheimer's disease (AD), despite being distinct disease entities, share numerous pathophysiological mechanisms such as those mediated by inflammation, immune exhaustion, and neurovascular unit compromise. An important shared mechanistic link is acute and chronic changes in protein kinase C (PKC) activity. PKC isoforms have widespread functions important for memory, blood-brain barrier maintenance, and injury repair that change as the body ages. Disease states accelerate PKC functional modifications. Mutated forms of PKC can contribute to neurodegeneration and cognitive decline. In some cases the PKC isoforms are still functional but are not successfully translocated to appropriate locations within the cell. The deficits in proper PKC translocation worsen stroke outcome and amyloid-β toxicity. Cross talk between the innate immune system and PKC pathways contribute to the vascular status within the aging brain. Unfortunately, comorbidities such as diabetes, obesity, and hypertension disrupt normal communication between the two systems. The focus of this review is to highlight what is known about PKC function, how isoforms of PKC change with age, and what additional alterations are consequences of stroke and AD. The goal is to highlight future therapeutic targets that can be applied to both the treatment and prevention of neurologic disease. Although the pathology of ischemic stroke and AD are different, the similarity in PKC responses warrants further investigation, especially as PKC-dependent events may serve as an important connection linking age-related brain injury.

Indexed as

Alzheimer DiseaseBrain IschemiaDisease ProgressionHumansNerve DegenerationProtein Kinase CStrokeProtein Kinase CAlzheimer's diseaseblood-brain barrierimmune exhaustioninnate immunityischemic strokeprotein kinase C

Identifiers

PMID25114088
PMCPMC4446718
OpenAlexW1598989069

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.