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Three major effects of APOE ε4 on Aβ immunotherapy induced ARIA
Foley KE, Wilcock DM.. Frontiers in aging neuroscience, 2024-05-02
Topic: Inflammation, microglia and astrocytes
The targeting of amyloid-beta (Aβ) plaques therapeutically as one of the primary causes of Alzheimer's disease (AD) dementia has been an ongoing effort spanning decades. While some antibodies are extremely promising and have been moved out of clinical trials and into the clinic, most of these treatments show similar adverse effects in the form of cerebrovascular damage known as amyloid-related imaging abnormalities (ARIA). The two categories of ARIA are of major concern for patients, families, and prescribing physicians, with ARIA-E presenting as cerebral edema, and ARIA-H as cerebral hemorrhages (micro- and macro-). From preclinical and clinical trials, it has been observed that the greatest genetic risk factor for AD, APOE ε4 , is also a major risk factor for anti-Aβ immunotherapy-induced ARIA. APOE ε4 carriers represent a large population of AD patients, and, therefore, limits the broad adoption of these therapies across the AD population. In this review we detail three hypothesized mechanisms by which APOE ε4 influences ARIA risk: (1) reduced cerebrovascular integrity, (2) increased neuroinflammation and immune dysregulation, and (3) elevated levels of CAA. The effects of APOE ε4 on ARIA risk is clear, however, the underlying mechanisms require more research.
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APA 7th
Foley, K. E., & Wilcock, D. M. (2024). Three major effects of APOE ε4 on Aβ immunotherapy induced ARIA. Frontiers in aging neuroscience. https://doi.org/10.3389/fnagi.2024.1412006
Vancouver
Foley KE, Wilcock DM. Three major effects of APOE ε4 on Aβ immunotherapy induced ARIA. Frontiers in aging neuroscience. 2024. doi:10.3389/fnagi.2024.1412006. PMID: 38756535.
BibTeX
@article{foley2024-38756535,
author = {Foley, K. E. and Wilcock, D. M.},
title = {{Three major effects of APOE ε4 on Aβ immunotherapy induced ARIA}},
journal = {Frontiers in aging neuroscience},
year = {2024},
doi = {10.3389/fnagi.2024.1412006},
pmid = {38756535},
url = {https://doi.org/10.3389/fnagi.2024.1412006}
}
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Key findings
- The two categories of ARIA are of major concern for patients, families, and prescribing physicians, with ARIA-E presenting as cerebral edema, and ARIA-H as cerebral hemorrhages (micro- and macro-).
- From preclinical and clinical trials, it has been observed that the greatest genetic risk factor for AD, APOE ε4 , is also a major risk factor for anti-Aβ immunotherapy-induced ARIA.
- APOE ε4 carriers represent a large population of AD patients, and, therefore, limits the broad adoption of these therapies across the AD population.
- In this review we detail three hypothesized mechanisms by which APOE ε4 influences ARIA risk: (1) reduced cerebrovascular integrity, (2) increased neuroinflammation and immune dysregulation, and (3) elevated levels of CAA.
- The effects of APOE ε4 on ARIA risk is clear, however, the underlying mechanisms require more research.
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Study details
- Evidence strengthLow
How this study scored 45/100
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 and multi-centre collaboration, so those were left out: it earned 26 of the 58 points we could judge it on, which is 45 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 | 4 / 5 | 2024 — within 3 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 38756535) |
| Free to read | 2 / 2 | Free to read |
| Points | 26 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 26 of the 58 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
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