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Pathogenetic pathways of cognitive dysfunction and dementia in metabolic syndrome
Yury Yu Borshchev, Yury P Uspensky, Michael M Galagudza. Life sciences, 2019-10-10
Topic: Gut, metabolism and diet
The prevalence of dementia worldwide is growing at an alarming rate. A number of studies and meta-analyses have provided evidence for increased risk of dementia in patients with metabolic syndrome (MS) as compared to persons without MS. However, there are some reports demonstrating a lack of association between MS and increased dementia risk. In this review, taking into account the potential role of individual MS components in the pathogenesis of MS-related cognitive dysfunction, we considered the underlying mechanisms in arterial hypertension, diabetes mellitus, dyslipidemia, and obesity. The pathogenesis of dementia in MS is multifactorial, involving both vascular injury and non-ischemic neuronal death due to neurodegeneration. Neurodegenerative and ischemic lesions do not simply coexist in the brain due to independent evolution, but rather exacerbate each other, leading to more severe consequences for cognition than would either pathology alone. In addition to universal mechanisms of cognitive dysfunction shared by all MS components, other pathogenetic pathways leading to cognitive deficits and dementia, which are specific for each component, also play a role. Examples of such component-specific pathogenetic pathways include central insulin resistance and hypoglycemia in diabetes, neuroinflammation and adipokine imbalance in obesity, as well as arteriolosclerosis and lipohyalinosis in arterial hypertension. A more detailed understanding of cognitive disorders based on the recognition of underlying molecular mechanisms will aid in the development of new methods for prevention and treatment of devastating cognitive problems in MS.
Key findings
- A number of studies and meta-analyses have provided evidence for increased risk of dementia in patients with metabolic syndrome (MS) as compared to persons without MS.
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Study details
- Study designmeta-analysis
- Evidence strengthHigh
How this study scored 68/100
Published in a peer-reviewed journal, and it is a meta-analysis pooling many studies. Scored zero for sample size, effect reported and studied in people because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 38 of the 56 points we could judge it on, which is 68 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Life sciences) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 12 / 12 | A meta-analysis pooling many studies |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 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) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31606384) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 38 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 38 of the 56 points we could judge it on is 68 out of 100. |
| Total | 68 / 100 | — |
What each of these 20 components measures, and what this score is not →
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APA 7th
Borshchev, Y. Y., Uspensky, Y. P., & Galagudza, M. M. (2019). Pathogenetic pathways of cognitive dysfunction and dementia in metabolic syndrome. Life sciences. https://doi.org/10.1016/j.lfs.2019.116932
Vancouver
Borshchev YY, Uspensky YP, Galagudza MM. Pathogenetic pathways of cognitive dysfunction and dementia in metabolic syndrome. Life sciences. 2019. doi:10.1016/j.lfs.2019.116932. PMID: 31606384.
BibTeX
@article{borshchev2019-31606384,
author = {Borshchev, Yury Yu and Uspensky, Yury P and Galagudza, Michael M},
title = {{Pathogenetic pathways of cognitive dysfunction and dementia in metabolic syndrome}},
journal = {Life sciences},
year = {2019},
doi = {10.1016/j.lfs.2019.116932},
pmid = {31606384},
url = {https://doi.org/10.1016/j.lfs.2019.116932}
}
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