Home › Research › TREM2 and immune genetics
Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target
Kulkarni B, Cruz-Martins N, Kumar D.. Molecular neurobiology, 2022-02-12
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is an ever more common neurodegenerative disease among the elderly, characterized by recurrent neuroinflammation and amyloid beta (Aβ) accumulation in the brain parenchyma. Recent genome-wide association studies (GWAS) have shown a distinct role for the innate immune system in AD, with microglia playing a key role. The function of microglial cells is stringently regulated by the neighboring microenvironment in the brain. Upon interruption in diseases, like AD, it demonstrates neurotoxic and neuroprotective action by M1 (neurotoxic) and M2 (neuroprotective) microglial phenotypes, respectively, in the brain. Microglial cells on activation by complement factors, toll-like receptors, and genetic variants result in Aβ' phagocytosis, synaptic pruning, and reactivation of complement pathway. Recent studies have demonstrated the presence of potential therapeutic targets in microglial cells. Immune receptors revealed on microglia as potential drug targets can be paired immunoglobulin-like type 2 receptor (PILR), CD3358, and triggering receptor expressed on myeloid cells 2 (TREM2), as they can have impact on late-onset AD occurrence and progression. Thus, targeting these receptors can accentuate the beneficial effects of microglial cells required to decelerate the progression of AD. This review emphasizes the microglial phenotypes, its function in AD brain, and potential immunological and therapeutic targets to fight this highly progressive neurodegenerative disorder.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Kulkarni, B., Cruz-Martins, N., & Kumar, D. (2022). Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target. Molecular neurobiology. https://doi.org/10.1007/s12035-021-02661-x
Vancouver
Kulkarni B, Cruz-Martins N, Kumar D. Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target. Molecular neurobiology. 2022. doi:10.1007/s12035-021-02661-x. PMID: 35149973.
BibTeX
@article{kulkarni2022-35149973,
author = {Kulkarni, B. and Cruz-Martins, N. and Kumar, D.},
title = {{Microglia in Alzheimer's Disease: An Unprecedented Opportunity as Prospective Drug Target}},
journal = {Molecular neurobiology},
year = {2022},
doi = {10.1007/s12035-021-02661-x},
pmid = {35149973},
url = {https://doi.org/10.1007/s12035-021-02661-x}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Microglial cells on activation by complement factors, toll-like receptors, and genetic variants result in Aβ' phagocytosis, synaptic pruning, and reactivation of complement pathway.
- Recent studies have demonstrated the presence of potential therapeutic targets in microglial cells.
- Immune receptors revealed on microglia as potential drug targets can be paired immunoglobulin-like type 2 receptor (PILR), CD3358, and triggering receptor expressed on myeloid cells 2 (TREM2), as they can have impact on late-onset AD occurrence and progression.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 40/100
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 23 of the 58 points we could judge it on, which is 40 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular 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 | 3 / 5 | 2022 — 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) |
| 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 35149973) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 23 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 23 of the 58 points we could judge it on is 40 out of 100. |
| Total | 40 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.
Related studies in TREM2 and immune genetics
Also tagged “drug-target”
4 studies in the library carry the topic tag “drug-target”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 4 tagged studies.