27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Accurate diagnosis of frontotemporal dementia (FTD) with right anterior temporal lobe (RATL) predominance remains challenging due to lack of clinical characterization, and standardized terminology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The drive for positive social interactions, or "social rewards", is an important motivator of human behaviour, conferring several adaptive benefits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI) is a clinical condition with a high risk of progression to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The subcellular localization of organelles, mRNAs and proteins is particularly challenging in neurons. 4 key findings →
Evidence: low
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Patients with PDD showed a more severe phenotype than those with DLB, with higher scores in motor severity, hallucinations, delusions, somnolence, and urinary dysfunction (all p≤0.01). 5 key findings →
Participants: 31 Evidence: low
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Four themes described current primary care practitioner practices in dementia diagnosis and management (1) Family concern triggers dementia investigation (2) GPs delay conversations about dementia (3) Completing routine cognitive assessments in the 75+ health assessment, and (4) Variability in post-diagnostic care. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundCurrent physical activity literature does not distinguish between young (dementia diagnosed before 65) and late onset dementia despite differences between these groups such as age, being known to influence physical activity levels. 1 key finding →
Design: cross-sectional Participants: 23 Evidence: low
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Alzheimer's disease (AD) is characterized by the hallmark pathologies of β-amyloid plaques and neurofibrillary tangles (NFTs), which vary across brain regions and between affected individuals. 2 key findings →
Evidence: low
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Several concepts, which in the aggregate get might be used to account for "resilience" against age- and disease-related changes, have been the subject of much research.
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Down syndrome, caused by the trisomy of chromosome 21, is a complex condition characterized by a number of phenotypic features, including reduced neuron number and synaptic plasticity, early Alzheimer disease-like neurodegeneration, craniofacial dysmorphia, heart development defects, increased incidence of childhood leukemia, and powerful suppression of the incidence of most solid tumors. 3 key findings →
Participants: 1,661 Evidence: low
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26% of the participants experienced delirium prior to diagnosis of DLB, with one participant experiencing multiple episodes in the 24 months before diagnosis. 5 key findings →
Evidence: low
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Four GPs and eleven physicians were interviewed, and four major themes emerged: (1) knowledge of best practices of BPSD management, (2) awareness of current challenges in BPSD management, (3) non-involvement, blame shifting and rationalisation: perceived reasons for the current challenges and (4) suggested solutions. 5 key findings →
Evidence: low
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Obstructive sleep apnoea (OSA) is increasingly recognised as a significant risk factor for cognitive decline and dementia. 1 key finding →
Evidence: low
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Of 142 respondents, 53% supported, 10% were uncertain, and 37% opposed legalizing euthanasia for terminal illness with severe symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To the Editor: MC1 is a monoclonal anti-tau antibody developed by the Peter Davies laboratory in the 1990s to aid the neuropathological diagnosis of Alzheimer disease (AD).1 Raised against Alz-50-immunopurified paired helical filaments (PHFs) from an AD brain, MC1 recognizes a conformational, discontinuous epitope involving residues 7-9 in the N-terminus and 313-322 in the third repeat domain of tau (Figure 1A). 1 key finding →
Evidence: moderate
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These inputs and activities were shown in the logic model to result in short, medium, and long-term outcomes, including reduced healthcare resource use and increased quality of life for people with dementia at the end of life. 2 key findings →
Participants: 18 Evidence: low
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Alzheimer type II astrocytosis is the pathological hallmark of hepatic encephalopathy. 3 key findings →
Evidence: low
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The participant demonstrated 28.6% mastery of the grocery shopping task. 4 key findings →
Evidence: low
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Six key themes were identified: Inadequate preparation, guidance and access to appropriate resources; Taboo and misunderstanding: talking about death; Dementia as a terminal illness and the role of palliative care; Key time points, critical events and decisions; Planning ahead not in reality; Family issues and dynamics. 5 key findings →
Evidence: low
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Dementia and hearing loss are both highly prevalent conditions among older adults. 4 key findings →
Design: cohort study Participants: 25 Evidence: moderate
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Parkinsons disease and dementia with Lewy bodies patients both demonstrated weaker global BOLD-CSF coupling compared to controls, with no detectable difference between patient groups. 4 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →