27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Disease-specific patterns of functional network topology and connectivity alterations were observed in patients with EOAD and bvFTD. 3 key findings →
Participants: 37 Evidence: low
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Diffusion tensor imaging (DTI) based assessment of white matter fiber tract integrity can support the diagnosis of Alzheimer's disease (AD). 4 key findings →
Participants: 137 Evidence: low
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Cognitive impairment is an increasingly recognized major cause of chronic disability and is commonly found in patients with chronic kidney disease (CKD). 3 key findings →
Evidence: low
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Over the last decade, age-standardised dementia incidence estimated rates have decreased by 52.8 % for women and 53.1 % for males. 5 key findings →
Design: cohort study Evidence: moderate
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We identified 132,968 individuals, of whom 12,088 with severe Zoster, 60,440 matched controls among the general population, and 60,440 matched controls among the hospitalised population. 5 key findings →
Participants: 132,968 Evidence: moderate
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Due to the COVID-19 pandemic, most memory clinics have had to suspend their activities. 5 key findings →
Evidence: low
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These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD. 3 key findings →
Evidence: low
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Identifying pre-clinical Alzheimer's disease (AD) in subjects with mild cognitive impairment (MCI) is a major issue in clinical diagnosis. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) and frontotemporal dementia (FTD) are leading causes of cognitive decline. 4 key findings →
Design: cross-sectional Evidence: low
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This paper reviews current knowledge on sleep problems, sleep architecture changes and quantitative EEG alteration brought on by various neurodegenerative diseases, such as Alzheimer's disease (AD), progressive supranuclear palsy (PSP), REM sleep behavior disorder (RBD), Parkinson's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy MSA, Huntington's disease and Creutzfeldt-Jakob disease, in comparison to normal aging. 2 key findings →
Evidence: low
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At baseline, sbvFTD showed right-predominant temporal pole involvement associated with significant right frontal atrophy. 5 key findings →
Design: longitudinal study Evidence: moderate
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Microglial MVs are neurotoxic and myelinotoxic in the presence of Aβ1-42 . 4 key findings →
Evidence: low
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• SCD patients showed attenuation of sensory (P1, N1, P2) and cognitive (P300, P600, P900) components, with performance-related gains. • MCI patients exhibited neural compensations, reversing the downward trend observed in SCD, which resulted in a non-monotonic pattern of ERPs. • The progression of cognitive decline was linked to electrophysiological discontinuity, suggesting resilience mechanisms in both low and higher order cognitive regions. 5 key findings →
Participants: 178 Evidence: moderate
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Triggering receptor expressed in myeloid (TREM) cells 2, a receptor expressed by myeloid cells, osteoclasts and microglia, is known to play a protective role in bones and brain. 4 key findings →
Evidence: low
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From 356 participants, 104 were MCI-C, whereas 252 were MCI-NC. 5 key findings →
Participants: 356 Evidence: low
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Dementia developed in 104 individuals (29.6%), including 85 (22.4%) who met core clinical criteria for probable and possible Alzheimer's disease dementia. 3 key findings →
Participants: 398 Evidence: low
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Together with its adaptor protein, the adaptor protein of 12 kDa also known as KARAP and TYROBP (DAP12), triggering receptor expressed in myeloid cells 2 (TREM2) is a stimulatory membrane receptor of the immunoglobulin/lectin-like superfamily, well known in myeloid cells. 4 key findings →
Evidence: low
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Differently from other myeloid cells, microglia derive exclusively from precursors originating within the yolk sac and migrate to the CNS under development, without any contribution from fetal liver or postnatal hematopoiesis. 4 key findings →
Evidence: low
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Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. 4 key findings →
Evidence: low
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This study highlights the role of age, gender, APOE genotype, and depressive symptoms in the presentation and progression of cognitive decline. 2 key findings →
Evidence: moderate
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Cognitive decline is a condition affecting almost one sixth of the elder population and is widely regarded as one of the first manifestations of Alzheimer's disease. 2 key findings →
Participants: 145 Evidence: moderate
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Aging is associated with an exaggerated response to peripheral inflammatory challenges together with behavioral and cognitive deficits. 4 key findings →
Evidence: low
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This joint Position Paper, developed by the Italian Expert Panel on Alzheimer convened by the Italian Society of Neurology with participation from multiple scientific societies, outlines strategic guidelines for reorganizing the patient journey in the era of anti-amyloid monoclonal antibodies for Alzheimer's disease. 1 key finding →
Evidence: low
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Microstructural alterations in brain tissue play a crucial role in the pathophysiology of frontotemporal dementia (FTD). 1 key finding →
Evidence: low
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Gender has an impact on CR, but not through socio‐economic variables. 2 key findings →
Participants: 440 Evidence: moderate
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →