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The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia
Folch J, Olloquequi J, Ettcheto M, Busquets O, Sánchez-López E, Cano A, Espinosa-Jiménez T, García ML et al.. Frontiers in aging neuroscience, 2019-09-06
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Nowadays, Alzheimer's disease (AD) is a severe sociological and clinical problem. Since it was first described, there has been a constant increase in its incidence and, for now, there are no effective treatments since current approved medications have only shown short-term symptomatic benefits. Therefore, it is imperative to increase efforts in the search for molecules and non-pharmacological strategies that are capable of slowing or stopping the progress of the disease and, ideally, to reverse it. The amyloid cascade hypothesis based on the fundamental role of amyloid has been the central hypothesis in the last 30 years. However, since amyloid-directed treatments have shown no relevant beneficial results other theories have been postulated to explain the origin of the pathology. The brain is a highly metabolically active energy-consuming tissue in the human body. It has an almost complete dependence on the metabolism of glucose and uses most of its energy for synaptic transmission. Thus, alterations on the utilization or availability of glucose may be cause for the appearance of neurodegenerative pathologies like AD. In this review article, the hypothesis known as Type 3 Diabetes (T3D) will be evaluated by summarizing some of the data that has been reported in recent years. According to published research, the adherence over time to low saturated fatty acids diets in the context of the Mediterranean diet would reduce the inflammatory levels in brain, with a decrease in the pro-inflammatory glial activation and mitochondrial oxidative stress. In this situation, the insulin receptor pathway would be able to fine tune the mitochondrial biogenesis in neuronal cells, regulation the adenosine triphosphate/adenosine diphosphate intracellular balance, and becoming a key factor involved in the preservation of the synaptic connexions and neuronal plasticity. In addition, new targets and strategies for the treatment of AD will be considered in this review for their potential as new pharmacological or non-pharmacological approaches.
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APA 7th
Folch, J., Olloquequi, J., Ettcheto, M., Busquets, O., Sánchez-López, E., Cano, A., et al. (2019). The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2019.00236
Vancouver
Folch J, Olloquequi J, Ettcheto M, Busquets O, Sánchez-López E, Cano A, et al. The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia. Frontiers in aging neuroscience. 2019. doi:10.3389/fnagi.2019.00236. PMID: 31551756.
BibTeX
@article{folch2019-31551756,
author = {Folch, J. and Olloquequi, J. and Ettcheto, M. and Busquets, O. and Sánchez-López, E. and Cano, A. and Espinosa-Jiménez, T. and García, M. L. and others},
title = {{The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer's Dementia}},
journal = {Frontiers in aging neuroscience},
year = {2019},
doi = {10.3389/fnagi.2019.00236},
pmid = {31551756},
url = {https://doi.org/10.3389/fnagi.2019.00236}
}
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Key findings
- However, since amyloid-directed treatments have shown no relevant beneficial results other theories have been postulated to explain the origin of the pathology.
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Study details
- Evidence strengthLow
How this study scored 41/100
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. 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 and multicenter collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in aging neuroscience) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31551756) |
| Free to read | 2 / 2 | Free to read |
| Points | 24 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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