27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
At randomization, the mean age is 72, 50% female, 77% with CDR-global score 0.5, and mean MMSE score 23.8. 5 key findings →
Design: clinical trial Participants: 464 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms. 2 key findings →
Participants: 108 Evidence: low
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The maximal tolerated dose of PQ912 has been identified and the results support future studies at still lower doses reaching > 50% target occupancy, a longer up-titration phase to potentially induce adaptation and longer treatment periods to confirm the early signals of efficacy as seen in this study. 4 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Cerebral deposition of amyloid beta peptide (Abeta) is an early and critical feature of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disorder characterized pathologically by ubiquitinated TAR DNA binding protein (TDP-43) inclusions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals. 1 key finding →
Design: randomized controlled trial Participants: 1,159 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study analyzed 80,660 single-nucleus transcriptomes from the prefrontal cortex of 48 individuals with varying degrees of Alzheimer's disease pathology to examine molecular and cellular changes across six major brain cell types. 4 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Tau hyperphosphorylation is an early step in tau-mediated neurodegeneration and is associated with intracellular aggregation of tau as neurofibrillary tangles, neuronal and synaptic loss, and eventual cognitive dysfunction in Alzheimer disease. 3 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this study, clinically normal adults with SNAP did not exhibit evidence of elevated tau levels, which suggests that this biomarker construct does not represent amyloid-independent tauopathy. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
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Researchers extracted soluble amyloid-beta protein oligomers directly from the cerebral cortex of subjects with Alzheimer's disease to study their impact. 3 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD. 5 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease.
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At baseline, Aβ+ participants showed higher CP FWf, increased white matter hyperintensity (WMH) volume, and decreased diffusion tensor image analysis along the perivascular space (DTI-ALPS). 5 key findings →
Design: cohort study Participants: 216 Evidence: moderate
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Despite continuing debate about the amyloid β-protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early, often initiating factor in Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Brain regions with higher synaptic density are associated with a higher 18F-AV-1451 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminishes with disease severity. 1 key finding →
Design: cross-sectional Participants: 12 Evidence: moderate
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The conservation of sleep across all animal species suggests that sleep serves a vital function.
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Alzheimer's disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ) production and clearance that leads to Aβ accumulation in the central nervous system (CNS).
Full summary, score breakdown and related studies → Original source Free full text
Full summary, score breakdown and related studies → Original source Free full text
This Primer conceptualizes Alzheimer disease (AD) as a genetic and sporadic neurodegenerative disorder driven by a complex interplay between loss of synaptic homeostasis and endosomal/lysosomal clearance pathway dysfunction, in which Aβ and tau products play key roles. 4 key findings →
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This study examined a transgenic mouse model in which human tau P301L overexpression was restricted to layer II of the entorhinal cortex (EC-II). 4 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a major cause of dementia and cognitive decline. 3 key findings →
Design: longitudinal study Evidence: moderate
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Traumatic brain injury (TBI) constitutes one of the strongest environmental risk factors for several progressive neurodegenerative disorders of cognitive impairment and dementia that are characterized by the pathological accumulation of hyperphosphorylated tau (p-Tau). 1 key finding →
Design: systematic review Evidence: high
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This study reviews recent advances in understanding the complex pathobiology of Alzheimer disease and discusses current treatment strategies. 3 key findings →
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= 0.009). Other neuropathologies were similar across cognitive groups. 4 key findings →
Design: cohort study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia is marked by progressive cognitive decline linked to oxidative stress, neuroinflammation, and synaptic dysfunction. 4 key findings →
Design: systematic review Participants: 29 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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.
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 →