Evidence map›Paper›PMID 24574966›Full record

ReviewFrontiers in cellular neuroscience2014

Insulin dysfunction and Tau pathology.

Noura B El Khoury, Maud Gratuze, Marie-Amélie Papon, Alexis Bretteville, Emmanuel Planel

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 128 citations in OpenAlex.

  1. Computerized Cognitive Training for Older Adults at Higher Dementia Risk due to Diabetes: Findings From a Randomized Controlled Trial.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020 · on this map
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1 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

5 authors at 1 institution in 1 country.

Noura B El KhouryDépartement de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
Maud GratuzeDépartement de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
Marie-Amélie PaponAxe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
Alexis BrettevilleAxe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
Emmanuel PlanelDépartement de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval Québec, QC, Canada ; Axe Neurosciences, Centre Hospitalier de l'Université Laval Québec, QC, Canada.
Centre hospitalier de l'Université Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neuropathological hallmarks of Alzheimer's disease (AD) include senile plaques of β-amyloid (Aβ) peptides (a cleavage product of the Amyloid Precursor Protein, or APP) and neurofibrillary tangles (NFT) of hyperphosphorylated Tau protein assembled in paired helical filaments (PHF). NFT pathology is important since it correlates with the degree of cognitive impairment in AD. Only a small proportion of AD is due to genetic variants, whereas the large majority of cases (~99%) is late onset and sporadic in origin. The cause of sporadic AD is likely to be multifactorial, with external factors interacting with biological or genetic susceptibilities to accelerate the manifestation of the disease. Insulin dysfunction, manifested by diabetes mellitus (DM) might be such factor, as there is extensive data from epidemiological studies suggesting that DM is associated with an increased relative risk for AD. Type 1 diabetes (T1DM) and type 2 diabetes (T2DM) are known to affect multiple cognitive functions in patients. In this context, understanding the effects of diabetes on Tau pathogenesis is important since Tau pathology show a strong relationship to dementia in AD, and to memory loss in normal aging and mild cognitive impairment. Here, we reviewed preclinical studies that link insulin dysfunction to Tau protein pathogenesis, one of the major pathological hallmarks of AD. We found more than 30 studies reporting Tau phosphorylation in a mouse or rat model of insulin dysfunction. We also payed attention to potential sources of artifacts, such as hypothermia and anesthesia, that were demonstrated to results in Tau hyperphosphorylation and could major confounding experimental factors. We found that very few studies reported the temperature of the animals, and only a handful did not use anesthesia. Overall, most published studies showed that insulin dysfunction can promote Tau hyperphosphorylation and pathology, both directly and indirectly, through hypothermia.

Indexed as

Alzheimer's diseasediabetes mellituskinasesphosphatasesTau phosphorylation

Identifiers

PMID24574966
PMCPMC3920186
OpenAlexW1978879182

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.