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npj Dementia is a peer-reviewed journal published by Springer Nature, covering Dementia and Cognitive Impairment Research, Alzheimer's disease research and treatments, Neuroinflammation and Neurodegeneration Mechanisms. Over its lifetime it has published 94 papers, which have received 174 citations.
| Publisher | Springer Nature |
|---|---|
| Reference style | Superscript numbered (Nature) Superscript — small raised numerals in the text 1. Smith, A., Jones, B. & Lee, C. A representative article title. npj Dementia 12, 45–58 (2023).
Formats any DOI in npj Dementia style. No sign-up. |
| Publishes research in | Dementia and Cognitive Impairment Research Alzheimer's disease research and treatments Neuroinflammation and Neurodegeneration Mechanisms Amyotrophic Lateral Sclerosis Research Machine Learning in Healthcare |
| Papers published last year | ≈49 |
| ISSN | 3005-1940 |
| Citation impact (2-yr) | 1.85 |
| h-index | 8 |
| i10-index | 5 |
| Top institutions publishing here | University of California, San Francisco |
| You get | A submission-ready PDF and the editable LaTeX source — ready to submit. |
Emerging evidence has established neuroinflammation as a primary driver of progressive neuronal loss observed across neurodegenerative diseases (NDDs). The NLRP3 inflammasome is a cytosolic immunoprotective danger sensing complex, which when aberrantly activated drives neuroinflammation, propagates amyloid deposition, and neurodegeneration. Herein, we report the therapeutic benefit of NLRP3 inflammasome inhibition in Alzheimer's disease (AD), using a…
Abstract Retrotransposons constitute over 40% of the human genome. Studies in Drosophila , mice, cultured cells, and human brain show that retrotransposons are activated in tauopathies, including Alzheimer’s disease, and causally drive neurodegeneration. The reverse transcriptase inhibitor 3TC (lamivudine) reduces retrotransposon activation and suppresses tau neurotoxicity among model systems. This phase 2a open-label trial (Pilot…
Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk. However, most prior analyses have not utilized longitudinal analyses or whole-brain neuroimaging biomarkers of AD. Herein, we employed longitudinal modeling and structural neuroimaging analyses to test the hypothesis that accelerated epigenetic aging would predict…
Abstract Variation in the APOE gene strongly affects Alzheimer’s disease (AD) risk. However, the proportion of AD burden attributable to this variation requires clarification, which would help to elucidate the scope of strategies targeting apolipoprotein E (APOE) for AD prevention and treatment. We estimated the extents to which clinically diagnosed AD, AD neuropathology and all-cause…
Abstract The relationship between sleep disorders and neurodegeneration is complex. Using >1 million electronic health records from Wales, UK, and Finland, we mined biobank data to identify relationships between sleep disorders and neurodegenerative diseases (NDDs). Additionally, we investigated how sleep-attributed risk may compensate for lack of NDD genetic risk. We found that sleep disorders were…
