27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
(1) To investigate the association between age at diabetes diagnosis and the incidence of all-cause dementia (ACD), Alzheimer’s disease (AD), and vascular dementia (VD) in individuals with diabetes. 4 key findings →
Evidence: moderate
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Diagnosis of LBD had high specificity but low sensitivity, with fewer than half of autopsy-confirmed cases having received an LBD diagnosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study examines the challenges caregivers face in interpreting the bodily behaviors of individuals with late-stage dementia as interactional signals. 5 key findings →
Evidence: low
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We identified three main themes of palliative hope in late-stage dementia: 1) Life is good and there is still time, 2) Agency and identity are not lost, and 3) Death will be good and professional support is available. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common cause of dementia in older adults, marked by a gradual and irreversible deterioration of cognitive abilities, including memory and thinking skills. 1 key finding →
Evidence: low
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IBC effectively ameliorates AD pathology through autophagy-mediated clearance of Aβ and suppressing neuroinflammation in 5x-FAD mice. 4 key findings →
Design: post-hoc analysis Evidence: low
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In particular, the severity of HIV-associated neurocognitive disorders (HAND) has been greatly reduced, significantly decreasing the prevalence of HIV-associated dementia [1]. 5 key findings →
Evidence: low
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Alzheimer disease (AD) is a debilitating progressive dementia, whose pathophysiology is not fully understood. 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common cause of dementia. 4 key findings →
Evidence: low
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Mild Cognitive Impairment (MCI) represents a critical stage between normal aging and dementia, with limited effective interventions currently available. 3 key findings →
Evidence: low
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Recent evidence indicates the presence of micro- and nanoplastics in the human brain, with higher accumulation observed in patients with dementia. 4 key findings →
Evidence: low
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Oxidative stress causes brain damage contributing to neurodegenerative and vascular diseases. 1 key finding →
Evidence: low
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The increase in senescent cells, including glial cells in the brain, is a general feature of normal aging and has been associated with age-related pathologies. 5 key findings →
Evidence: low
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In our study, steroid use delayed the progression of dementia. 3 key findings →
Participants: 459 Evidence: low
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Tauopathies, including Alzheimer's disease (AD) and Frontotemporal Dementia (FTD), are histopathologically defined by the aggregation of hyperphosphorylated pathological tau (pTau) as neurofibrillary tangles in the brain. 5 key findings →
Evidence: low
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GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. 2 key findings →
Evidence: low
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Tauopathies are neurodegenerative diseases characterized by accumulation of hyperphosphorylated tau protein (P-tau). 3 key findings →
Evidence: low
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In plasma, most complement analytes were not significantly different between spFTD and HC; the exceptions were C4 and FB, significantly decreased in spFTD vs HC ( p = 0.0192 and p = 0.0181, respectively), suggesting complement consumption in classical and alternative pathways. 3 key findings →
Participants: 20 Evidence: low
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In the AD continuum group, all cognitive test performances significantly correlated with tracer uptake, particularly in the left cortical areas. 4 key findings →
Participants: 120 Evidence: low
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The amyloid hypothesis is the predominant model of Alzheimer's disease (AD) pathogenesis, suggesting that amyloid beta (Aβ) peptide is the primary driver of neurotoxicity and a cascade of pathological events in the central nervous system. 1 key finding →
Evidence: low
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In this study, the rank of multifaceted activity of catechin (C), epicatechin (EC), epigallocatechin (EGC), epicatechin-3-gallate (ECG) and epigallocatechin-3-gallate (EGCG) was addressed. 1 key finding →
Evidence: low
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Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits. 1 key finding →
Evidence: low
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Tauopathies, including Alzheimer's disease and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), are characterized by the aberrant aggregation of tau protein into neurofibrillary tangles. 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most prevalent cause of dementia and can be conceptualized as a tauopathy initiated by the accumulation of amyloid-β (Aβ) in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The average MIND-NL scores for the short FFQ (8·4 ( sd 1·8) points) and food records (6·7 ( sd 1·7) points) showed to be significantly different ( P 0·20) were observed for 10 out of 15 MIND-NL diet components. 2 key findings →
Evidence: low
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →