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51/100

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Risk factors

Topic: Brain proteins, microglia and lab models

Metabolic syndrome (MetS) is a cluster of cardiovascular risk factors that includes obesity, diabetes, and dyslipidemia. Accumulating evidence implies that MetS contributes to the development and progression of Alzheimer's disease (AD); however, the factors connecting this association have not been determined. Insulin resistance (IR) is at the core of MetS and likely represent the key link between MetS and AD. In the central nervous system, insulin plays key roles in learning and memory, and AD patients exhibit impaired insulin signaling that is similar to that observed in MetS. As we face an alarming increase in obesity and T2D in all age groups, understanding the relationship between MetS and AD is vital for the identification of potential therapeutic targets. Recently, several diabetes therapies that enhance insulin signaling are being tested for a potential therapeutic benefit in AD and dementia. In this review, we will discuss MetS as a risk factor for AD, focusing on IR and the recent progress and future directions of insulin-based therapies.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Kim, B., & Feldman, E. L. (2015). Insulin resistance as a key link for the increased risk of cognitive impairment in the metabolic syndrome. Experimental & molecular medicine. https://doi.org/10.1038/emm.2015.3

Vancouver

Kim B, Feldman EL. Insulin resistance as a key link for the increased risk of cognitive impairment in the metabolic syndrome. Experimental & molecular medicine. 2015. doi:10.1038/emm.2015.3. PMID: 25766618.

BibTeX

@article{kim2015-25766618,
  author  = {Kim, B. and Feldman, E. L.},
  title   = {{Insulin resistance as a key link for the increased risk of cognitive impairment in the metabolic syndrome}},
  journal = {Experimental \& molecular medicine},
  year    = {2015},
  doi     = {10.1038/emm.2015.3},
  pmid    = {25766618},
  url     = {https://doi.org/10.1038/emm.2015.3}
}

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Key findings

Insulin resistance (IR) is at the core of MetS and likely represent the key link between MetS and AD.
In the central nervous system, insulin plays key roles in learning and memory, and AD patients exhibit impaired insulin signaling that is similar to that observed in MetS.
As we face an alarming increase in obesity and T2D in all age groups, understanding the relationship between MetS and AD is vital for the identification of potential therapeutic targets.
Recently, several diabetes therapies that enhance insulin signaling are being tested for a potential therapeutic benefit in AD and dementia.
In this review, we will discuss MetS as a risk factor for AD, focusing on IR and the recent progress and future directions of insulin-based therapies.

Why it matters

This review proposes insulin resistance as the key link between metabolic syndrome and Alzheimer's disease, noting that Alzheimer's patients show impaired insulin signaling similar to that in metabolic syndrome. It states that several diabetes therapies that enhance insulin signaling are being tested for potential benefit in Alzheimer's disease and dementia, so no treatment is established.

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Study details

Evidence strengthLow

How this study scored 51/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Experimental & molecular medicine)
Journal's citation record	2 / 4	Experimental & Molecular Medicine: journal h-index 181 (OpenAlex, 2026-10-29)
Study design	0 / 12	No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2015 — within 20 year(s) of the newest study here
Sample size	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	6 / 7	Cited 355 times (OpenAlex, 2026-10-10)
Citations per year	4 / 5	27.3 citations a year over 13 year(s) since 2015
Impact for its field and year	5 / 6	Cited 20.9× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 4 other studies in this library
Still being cited	3 / 4	Cited 93 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Eva L. Feldman: h-index 124 (OpenAlex, whole career)
Institution's track record	2 / 3	University of Michigan: institution h-index 2,240 (OpenAlex)
Multicenter collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 25766618)
Free to read	2 / 2	Free to read
Total	51 / 100	—

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