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Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease
Mikael Marttinen, Mari Takalo, Teemu Natunen, Rebekka Wittrahm, Sami Gabbouj, Susanna Kemppainen, Ville Leinonen, Heikki Tanila et al.. Frontiers in neuroscience, 2018-12-14
Topic: Inflammation, microglia and astrocytes
Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning. According to the prevailing amyloid cascade hypothesis of AD, increased soluble amyloid-β (Aβ) oligomer levels impair the synaptic functions and augment calcium dyshomeostasis, neuroinflammation, oxidative stress as well as the formation of neurofibrillary tangles at specific brain regions. Emerging new findings related to synaptic dysfunction and initial steps of neuroinflammation in AD have been able to delineate the underlying molecular mechanisms, thus reinforcing the development of new treatment strategies and biomarkers for AD beyond the conventional Aβ- and tau-targeted approaches. Particularly, the identification and further characterization of disease-associated microglia and their RNA signatures, AD-associated novel risk genes, neurotoxic astrocytes, and in the involvement of complement-dependent pathway in synaptic pruning and loss in AD have set the outstanding basis for further preclinical and clinical studies. Here, we discuss the recent development and the key findings related to the novel molecular mechanisms and targets underlying the synaptotoxicity and neuroinflammation in AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Marttinen, M., Takalo, M., Natunen, T., Wittrahm, R., Gabbouj, S., Kemppainen, S., et al. (2018). Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease. Frontiers in neuroscience. https://doi.org/10.3389/fnins.2018.00963
Vancouver
Marttinen M, Takalo M, Natunen T, Wittrahm R, Gabbouj S, Kemppainen S, et al. Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease. Frontiers in neuroscience. 2018. doi:10.3389/fnins.2018.00963. PMID: 30618585.
BibTeX
@article{marttinen2018-30618585,
author = {Marttinen, Mikael and Takalo, Mari and Natunen, Teemu and Wittrahm, Rebekka and Gabbouj, Sami and Kemppainen, Susanna and Leinonen, Ville and Tanila, Heikki and others},
title = {{Molecular Mechanisms of Synaptotoxicity and Neuroinflammation in Alzheimer's Disease}},
journal = {Frontiers in neuroscience},
year = {2018},
doi = {10.3389/fnins.2018.00963},
pmid = {30618585},
url = {https://doi.org/10.3389/fnins.2018.00963}
}
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Key findings
- Alzheimer's disease (AD) is the most common neurodegenerative disorder, which is clinically associated with a global cognitive decline and progressive loss of memory and reasoning.
Study details
- Evidence strengthLow
How this study scored 39/100
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 22 of the 56 points we could judge it on, which is 39 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in 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 | 2 / 5 | 2018 — 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 30618585) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 22 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 22 of the 56 points we could judge it on is 39 out of 100. |
| Total | 39 / 100 | — |
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