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Molecular neuropathology of frontotemporal dementia: insights into disease mechanisms from postmortem studies
Mackenzie IR, Neumann M.. Journal of neurochemistry, 2016-06-15
Topic: Brain proteins, microglia and lab models
Frontotemporal dementia (FTD) is a clinical syndrome with a heterogeneous molecular basis. The past decade has seen the discovery of several new FTD-causing genetic mutations and the identification of many of the relevant pathological proteins. The current neuropathological classification is based on the predominant protein abnormality and allows most cases of FTD to be placed into one of three broad molecular subgroups; frontotemporal lobar degeneration with tau, TDP-43 or FET protein accumulation.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mackenzie, I. R., & Neumann, M. (2016). Molecular neuropathology of frontotemporal dementia: insights into disease mechanisms from postmortem studies. Journal of neurochemistry. https://doi.org/10.1111/jnc.13588
Vancouver
Mackenzie IR, Neumann M. Molecular neuropathology of frontotemporal dementia: insights into disease mechanisms from postmortem studies. Journal of neurochemistry. 2016. doi:10.1111/jnc.13588. PMID: 27306735.
BibTeX
@article{mackenzie2016-27306735,
author = {Mackenzie, I. R. and Neumann, M.},
title = {{Molecular neuropathology of frontotemporal dementia: insights into disease mechanisms from postmortem studies}},
journal = {Journal of neurochemistry},
year = {2016},
doi = {10.1111/jnc.13588},
pmid = {27306735},
url = {https://doi.org/10.1111/jnc.13588}
}
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
- The past decade has seen the discovery of several new FTD-causing genetic mutations and the identification of many of the relevant pathological proteins.
- The current neuropathological classification is based on the predominant protein abnormality and allows most cases of FTD to be placed into one of three broad molecular subgroups; frontotemporal lobar degeneration with tau, TDP-43 or FET protein accumulation.
- This review will describe our current understanding of the molecular basis of FTD, focusing on insights gained from the study of human postmortem tissue, as well as some of the current controversies.
- Most cases of FTD can be subclassified into one of three broad molecular subgroups based on the predominant protein that accumulates as pathological cellular inclusions.
Why it matters
This review describes how frontotemporal dementia cases can be grouped by which protein accumulates in the brain, including tau, TDP-43, or FET proteins. It concerns frontotemporal dementia, not Alzheimer's disease, and does not report any treatment, cure, or prevention for Alzheimer's.
Study details
- Evidence strengthLow
How this study scored 51/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neurochemistry) |
| Journal's citation record | 3 / 4 | Journal of Neurochemistry: journal h-index 349 (OpenAlex, 2026-10-29) |
| 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 | 1 / 5 | 2016 — within 20 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 | 6 / 7 | Cited 382 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 31.8 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 5 / 6 | Cited 21.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 13 other studies in this library |
| Still being cited | 3 / 4 | Cited 90 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Manuela Neumann: h-index 90 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of British Columbia: institution h-index 1,424 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27306735) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/jnc.13588
- PubMed: 27306735
- Original source →
- Free full text: Journal of Neurochemistry →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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