Evidence map›Paper›PMID 33728019›Full record

ReviewOxidative medicine and cellular longevity2021

Pathology, Risk Factors, and Oxidative Damage Related to Type 2 Diabetes-Mediated Alzheimer's Disease and the Rescuing Effects of the Potent Antioxidant Anthocyanin.

Muhammad Sohail Khan, Muhammad Ikram, Tae Ju Park, Myeong Ok Kim

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.0field-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

17 citing papers in PubMed, 43 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

4 authors at 2 institutions in 2 countries.

Muhammad Sohail KhanDivision of Life Science and Applied Life Science (BK 21), College of Natural Sciences, Gyeongsang National University, Jinju 52828, Republic of Korea.ORCID https://orcid.org/0000-0003-4902-4698
Muhammad IkramDivision of Life Science and Applied Life Science (BK 21), College of Natural Sciences, Gyeongsang National University, Jinju 52828, Republic of Korea.ORCID https://orcid.org/0000-0001-5226-4081
Tae Ju ParkHaemato-oncology/Systems Medicine Group, Paul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, MVLS, University of Glasgow, UK.
Myeong Ok KimDivision of Life Science and Applied Life Science (BK 21), College of Natural Sciences, Gyeongsang National University, Jinju 52828, Republic of Korea.ORCID https://orcid.org/0000-0003-4317-1072
Gyeongsang National University · KRBlood Cancer UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathology and neurodegeneration in type 2 diabetes- (T2D-) mediated Alzheimer's disease (AD) have been reported in several studies. Despite the lack of information regarding the basic underlying mechanisms involved in the development of T2D-mediated AD, some common features of the two conditions have been reported, such as brain atrophy, reduced cerebral glucose metabolism, and insulin resistance. T2D phenotypes such as glucose dyshomeostasis, insulin resistance, impaired insulin signaling, and systemic inflammatory cytokines have been shown to be involved in the progression of AD pathology by increasing amyloid-beta accumulation, tau hyperphosphorylation, and overall neuroinflammation. Similarly, oxidative stress, mitochondrial dysfunction, and the generation of advanced glycation end products (AGEs) and their receptor (RAGE) as a result of chronic hyperglycemia may serve as critical links between diabetes and AD. The natural dietary polyflavonoid anthocyanin enhances insulin sensitivity, attenuates insulin resistance at the level of the target tissues, inhibits free fatty acid oxidation, and abrogates the release of peripheral inflammatory cytokines in obese (prediabetic) individuals, which are responsible for insulin resistance, systemic hyperglycemia, systemic inflammation, brain metabolism dyshomeostasis, amyloid-beta accumulation, and neuroinflammatory responses. In this review, we have shown that obesity may induce T2D-mediated AD and assessed the recent therapeutic advances, especially the use of anthocyanin, against T2D-mediated AD pathology. Taken together, the findings of current studies may help elucidate a new approach for the prevention and treatment of T2D-mediated AD by using the polyflavonoid anthocyanin.

Indexed as

Oxidative StressAlzheimer DiseaseAnimalsAnthocyaninsAntioxidantsDiabetes Mellitus, Type 2HumansRisk FactorsAnthocyaninsAntioxidants

Identifiers

PMID33728019
PMCPMC7936905
OpenAlexW3134710509

What Socratic 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 Socratic graph.