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BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology
Liansheng Zhang, Yun Qian, Jie Li, Xuan Zhou, He Xu, Jie Yan, Jialing Xiang, Xiang Yuan et al.. iScience, 2021-08-04
Topic: Inflammation, microglia and astrocytes
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. However, the underlying molecular mechanism is incompletely understood. Here we report that the pro-apoptotic protein BAD as a key regulator for neuronal apoptosis, neuroinflammation and Aβ clearance in AD. BAD pro-apoptotic activity is significantly increased in neurons of AD patients and 5XFAD mice. Conversely, genetic disruption of Bad alleles restores spatial learning and memory deficits in 5XFAD mice. Mechanistically, phosphorylation and inactivation of BAD by neurotropic factor-activated Akt is abrogated in neurons under AD condition. Through reactive oxygen species (ROS)-oxidized mitochondrial DNA (mtDNA) axis, BAD also promotes microglial NLRP3 inflammasome activation, thereby skewing microglia toward neuroinflammatory microglia to inhibit microglial phagocytosis of Aβ in AD mice. Our results support a model in which BAD contributes to AD pathologies by driving neuronal apoptosis and neuroinflammation but suppressing microglial phagocytosis of Aβ, suggesting that BAD is a potential therapeutic target for AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zhang, L., Qian, Y., Li, J., Zhou, X., Xu, H., Yan, J., et al. (2021). BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology. iScience. https://doi.org/10.1016/j.isci.2021.102942
Vancouver
Zhang L, Qian Y, Li J, Zhou X, Xu H, Yan J, et al. BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology. iScience. 2021. doi:10.1016/j.isci.2021.102942. PMID: 34430820.
BibTeX
@article{zhang2021-34430820,
author = {Zhang, Liansheng and Qian, Yun and Li, Jie and Zhou, Xuan and Xu, He and Yan, Jie and Xiang, Jialing and Yuan, Xiang and others},
title = {{BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology}},
journal = {iScience},
year = {2021},
doi = {10.1016/j.isci.2021.102942},
pmid = {34430820},
url = {https://doi.org/10.1016/j.isci.2021.102942}
}
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Key findings
- BAD pro-apoptotic activity is significantly increased in neurons of AD patients and 5XFAD mice.
- Our results support a model in which BAD contributes to AD pathologies by driving neuronal apoptosis and neuroinflammation but suppressing microglial phagocytosis of Aβ, suggesting that BAD is a potential therapeutic target for 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 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, multicenter 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 (iScience) |
| 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) |
| 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 34430820) |
| 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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