Evidence map›Paper›PMID 25673434›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2015

The metabolism hypothesis of Alzheimer's disease: from the concept of central insulin resistance and associated consequences to insulin therapy.

Katrin Morgen, Lutz Frölich

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 42 citations in OpenAlex.

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  7. In vivo methods for imaging blood-brain barrier function and dysfunction.European journal of nuclear medicine and molecular imaging · 2023
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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

2 authors at 1 institution in 1 country.

Katrin MorgenCentral Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, J5, 68159, Mannheim, Germany, Katrin.Morgen@zi-mannheim.de.
Lutz Frölich
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The concept of central insulin resistance and dysfunctional insulin signaling in Alzheimer's disease (AD) has been developed by Siegfried Hoyer in 1985-2000. It is widely recognized that a cerebrometabolic deficiency is one of the most relevant proximate characteristics of sporadic AD, including functional deficits in oxidative glucose breakdown, oxidative stress and amplifying the action of glucocorticoids in the brain. Insulin and insulin receptors are widely distributed in the brain and are impaired in the post-mortem Alzheimer brain. Functionally, altered insulin signaling may promote synaptic dysfunction and impaired connectivity, especially in highly connected and metabolically active regions of the brain, which in turn predisposes towards AD pathology. Thus, the hypothesis has been proposed that defects in the brain insulin signal transduction system and associated consequences, e.g., oxidative stress, are centrally involved in the etiopathogenesis of sporadic AD. Most importantly, in a research field still awaiting substantial progress in therapeutic options, the idea of AD as a brain type of diabetes mellitus is now being translated into clinical trials with promising early results.

Indexed as

Alzheimer DiseaseAnimalsBrainGlucoseHumansInsulinInsulin ResistanceNootropic AgentsGlucoseInsulinNootropic Agents

Identifiers

PMID25673434
OpenAlexW2003776455

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.