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The Neurovascular Unit Dysfunction in Alzheimer's Disease
Luis O Soto-Rojas, Mar Pacheco-Herrero, Paola A Martínez-Gómez, B Berenice Campa-Córdoba, Ricardo Apátiga-Pérez, Marcos M Villegas-Rojas, Charles R Harrington, Fidel de la Cruz et al.. International journal of molecular sciences, 2021-02-18
Topic: Inflammation, microglia and astrocytes
Alzheimer's disease (AD) is the most common neurodegenerative disease worldwide. Histopathologically, AD presents with two hallmarks: neurofibrillary tangles (NFTs), and aggregates of amyloid β peptide (Aβ) both in the brain parenchyma as neuritic plaques, and around blood vessels as cerebral amyloid angiopathy (CAA). According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia. Hypoxia may reduce Aβ clearance from the brain and increase its production, leading to both parenchymal and vascular accumulation of Aβ. An increase in Aβ amplifies neuronal dysfunction, NFT formation, and accelerates neurodegeneration, resulting in dementia. In recent decades, therapeutic approaches have attempted to decrease the levels of abnormal Aβ or tau levels in the AD brain. However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition. Here, we review the pathogenesis and potential therapeutic targets associated with dysfunction of the NVU in AD.
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APA 7th
Soto-Rojas, L. O., Pacheco-Herrero, M., Martínez-Gómez, P. A., Campa-Córdoba, B. B., Apátiga-Pérez, R., Villegas-Rojas, M. M., et al. (2021). The Neurovascular Unit Dysfunction in Alzheimer's Disease. International journal of molecular sciences. https://doi.org/10.3390/ijms22042022
Vancouver
Soto-Rojas LO, Pacheco-Herrero M, Martínez-Gómez PA, Campa-Córdoba BB, Apátiga-Pérez R, Villegas-Rojas MM, et al. The Neurovascular Unit Dysfunction in Alzheimer's Disease. International journal of molecular sciences. 2021. doi:10.3390/ijms22042022. PMID: 33670754.
BibTeX
@article{sotorojas2021-33670754,
author = {Soto-Rojas, Luis O and Pacheco-Herrero, Mar and Martínez-Gómez, Paola A and Campa-Córdoba, B Berenice and Apátiga-Pérez, Ricardo and Villegas-Rojas, Marcos M and Harrington, Charles R and de la Cruz, Fidel and others},
title = {{The Neurovascular Unit Dysfunction in Alzheimer's Disease}},
journal = {International journal of molecular sciences},
year = {2021},
doi = {10.3390/ijms22042022},
pmid = {33670754},
url = {https://doi.org/10.3390/ijms22042022}
}
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Key findings
- According to the vascular hypothesis of AD, vascular risk factors can result in dysregulation of the neurovascular unit (NVU) and hypoxia.
- However, several of these approaches have either been associated with an inappropriate immune response triggering inflammation, or have failed to improve cognition.
- Here, we review the pathogenesis and potential therapeutic targets associated with dysfunction of the NVU in AD.
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 randomised / 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, multi-centre collaboration and free to read, so those were left out: it earned 23 of the 56 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International journal of molecular sciences) |
| 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 | 3 / 5 | 2021 — within 6 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 | No randomisation 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 33670754) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 23 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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