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Evidence for pathophysiological commonalities between metabolic and neurodegenerative diseases
Hölscher C.. International review of neurobiology, 2020-08-11
Topic: Brain proteins, microglia and lab models
Diabetes mellitus is a risk factor for developing neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. This relationship seems counter-intuitive as these pathological syndromes appear to be very different. However, they share underlying mechanisms such as desensitization of insulin signaling. Insulin not only regulates blood glucose levels, but also acts as a growth factor that is important for neuronal activity and repair. Insulin signaling desensitization has been found in the brains of people with progressive neurodegenerative diseases, which is most likely driven by chronic inflammation. Based on this, insulin has been tested in patients with Alzheimer's disease, and it was found that memory formation was improved and brain pathology reduced. Glucagon-like peptide-1 (GLP-1) is an incretin hormone, and numerous drugs that mimic this peptide are on the market to treat type 2 diabetes mellitus. Preclinical studies have provided robust evidence that some of these drugs, such as liraglutide or lixisenatide can enter the brain and improve key pathological parameters, such as memory loss, impairment of motor activity, synapse loss, reduced energy utilization by neurons and chronic inflammation in the brain. First clinical trials with a GLP-1 mimetic show good effects in patients with Parkinson's disease, improving motor control and insulin signaling in the brain. This is a proof of concept that this approach is viable and that drug treatment affects the main drivers of the disease and does not just modify the symptoms. It demonstrates that this new research area is a promising and fertile space for the development of novel treatments for neurodegenerative diseases.
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APA 7th
Hölscher, C. (2020). Evidence for pathophysiological commonalities between metabolic and neurodegenerative diseases. International review of neurobiology. https://doi.org/10.1016/bs.irn.2020.01.007
Vancouver
Hölscher C. Evidence for pathophysiological commonalities between metabolic and neurodegenerative diseases. International review of neurobiology. 2020. doi:10.1016/bs.irn.2020.01.007. PMID: 32854859.
BibTeX
@article{holscher2020-32854859,
author = {Hölscher, C.},
title = {{Evidence for pathophysiological commonalities between metabolic and neurodegenerative diseases}},
journal = {International review of neurobiology},
year = {2020},
doi = {10.1016/bs.irn.2020.01.007},
pmid = {32854859},
url = {https://doi.org/10.1016/bs.irn.2020.01.007}
}
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Key findings
- Glucagon-like peptide-1 (GLP-1) is an incretin hormone, and numerous drugs that mimic this peptide are on the market to treat type 2 diabetes mellitus.
- Preclinical studies have provided robust evidence that some of these drugs, such as liraglutide or lixisenatide can enter the brain and improve key pathological parameters, such as memory loss, impairment of motor activity, synapse loss, reduced energy utilization by neurons and chronic inflammation in the brain.
- First clinical trials with a GLP-1 mimetic show good effects in patients with Parkinson's disease, improving motor control and insulin signaling in the brain.
- This is a proof of concept that this approach is viable and that drug treatment affects the main drivers of the disease and does not just modify the symptoms.
- It demonstrates that this new research area is a promising and fertile space for the development of novel treatments for neurodegenerative diseases.
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Study details
- Evidence strengthLow
How this study scored 38/100
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 22 of the 58 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International review of neurobiology) |
| 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 | 2020 — 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 32854859) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 22 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 22 of the 58 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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