30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
MEG 16-38Hz spectral power, particularly over parieto-occipital magnetometers, was significantly reduced in the AD progression group. 5 key findings →
Participants: 117 Evidence: low
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In PD‐SCD, baseline CSF Aβ42 is associated with cognitive progression. 5 key findings →
Design: cohort study Participants: 50 Evidence: moderate
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The rate of reversion from MCI to normal cognition was 37.0% after 2 years and 32.9% after 12 years. 5 key findings →
Design: longitudinal study Participants: 1,262 Evidence: moderate
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Cross-sectional studies suggest a limited relationship between accelerated epigenetic aging derived from epigenetic clocks, and Alzheimer's disease (AD) pathophysiology or risk. 3 key findings →
Design: cross-sectional Evidence: moderate
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Alzheimer’s disease (AD), a leading neurodegenerative disorder, progresses from an intermediary stage known as Mild Cognitive Impairment (MCI), characterized by measurable cognitive decline with retained functional independence. 1 key finding →
Design: longitudinal study Evidence: moderate
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Detecting Alzheimer's disease (AD) in its earliest stages, particularly during an onset of Mild Cognitive Impairment (MCI), remains challenging due to the overlap of initial symptoms with normal aging processes. 3 key findings →
Participants: 78 Evidence: low
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In the MCI+NPS group, the most frequently endorsed NPS was anxiety (46.2 %), the less prevalent NPS was euphoria/elation (1.44 %). 5 key findings →
Design: cross-sectional Participants: 376 Evidence: low
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All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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Among 558 amnestic MCI participants (168 ChEI users), ChEI users exhibited higher risk of progression to AD dementia (hazard ratio = 1.77, 95% confidence interval: 1.15 to 2.73, p = 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
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< 0.001). Shape features demonstrated the highest predictive accuracy for conversion, with areas under the curve of 0.891 at baseline and 0.898 at 2 years. 5 key findings →
Design: longitudinal study Participants: 180 Evidence: moderate
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The PD-MCI nonreversion group had greater p-tau:amyloid beta and t-tau:amyloid beta ratios relative to the PD-MCI reversion group. 4 key findings →
Design: longitudinal study Participants: 430 Evidence: moderate
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Thirteen studies were included (five guidelines, two clinical decisions, two systematic reviews, one meta-analysis, and three RCTs). 3 key findings →
Design: meta-analysis Evidence: high
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Our results highlight the prognostic value of biological AD staging. 5 key findings →
Participants: 492 Evidence: low
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= 0.005). Cox regression analysis revealed that polypharmacy was significantly associated with a reduced risk of MCI progression to dementia (hazard ratio [HR] = 0.49, 95% confidence interval [CI]: 0.31 to 0.78) after adjusting for covariates. 5 key findings →
Design: cohort study Evidence: moderate
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Mild cognitive impairment (MCI) is a clinical condition characterized by a decline in cognitive ability and progression of cognitive impairment. 3 key findings →
Participants: 239 Evidence: moderate
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Little is known about the dysbiosis of the gut microbiome in patients with mild cognitive impairment (MCI) potentially at risk for the development of Alzheimer's disease (AD). 5 key findings →
Design: cross-sectional Participants: 14 Evidence: moderate
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< 0.001). Receiver operating characteristic (ROC) analysis identified right hippocampal MD and t-tau as optimal classifiers for AD. 4 key findings →
Design: cross-sectional Evidence: low
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Key markers and mechanisms were identified for each stage: initial neurophysiological deficits in SCD with compensatory metabolomic responses, gut-brain axis dysregulation in MCI, and extensive metabolic disruption and multisystem breakdown in AD. 5 key findings →
Participants: 277 Evidence: low
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Neurophysiological activity features and tau pet provided additional information to the clinical model when acquired up to ∼4 years prior to diagnosis, but their accuracy decreased at larger intervals. 5 key findings →
Design: longitudinal study Participants: 102 Evidence: moderate
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This innovative study aims to test the feasibility of iTBS as a cognitive enhancement strategy in MCI. 3 key findings →
Participants: 20 Evidence: high
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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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Of the participants, 25, 92, and 61 were classified as cognitively normal, with mild cognitive impairment, and with dementia, respectively. 5 key findings →
Design: cohort study Evidence: moderate
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SSRI treatment showed no significant effect on AD dementia progression (hazard ratio = 1.64, 95% confidence interval: 0.61 to 4.38) or cognitive trajectories, regardless of AD pathology. 5 key findings →
Design: longitudinal study Evidence: moderate
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Dementia syndromes involve cognitive but also early motor impairment. 3 key findings →
Design: longitudinal study Participants: 104 Evidence: moderate
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The relation between vitamin A (VA) level and cognitive function and the underlying mechanisms have not been thoroughly investigated. 2 key findings →
Design: cross-sectional Participants: 1,817 Evidence: low
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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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events