27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our findings showed the strong predictive potential of PET, particularly florbetaben (FBB), which achieved an AUC of 0.84. 5 key findings →
Participants: 487 Evidence: low
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We found interactions between APOE4 and cognitive states in the aperiodic EEG exponent and the spectral power ratio (SPR). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overall, both machine learning techniques had an equivalent performance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings highlight hippocampal atrophy as a key pathway linking Aβ burden to cognitive impairment. 4 key findings →
Evidence: moderate
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The MMSE model achieves a mean absolute error (MAE) of 1.84 (95% CI: 1.64-2.04) internally and 2.19 in external validation. 5 key findings →
Evidence: moderate
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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →
Evidence: low
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Missense mutations in the amyloid precursor protein (APP) and presenilin-1 (PSEN1) cause early-onset familial Alzheimer’s disease (FAD) and alter proteolytic production of secreted 38-to-43-residue amyloid β-peptides (Aβ) by the PSEN1-containing γ-secretase complex, ostensibly supporting the amyloid hypothesis of pathogenesis. 3 key findings →
Evidence: low
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Amyloid precursor protein (APP) is a key player in various neuronal functions but also the source for toxic Aβ that accumulates in the brain of Alzheimer patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The sample included 61 participants (55.7% female), aged 18-58, with a median education of 12 years (IQR: 10-14). 5 key findings →
Participants: 61 Evidence: low
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In previous studies, we isolated a series of novel gentisides with nerve growth factor (NGF)-mimic activities from Gentiana rigescens Franch and conducted continuous structure–activity relationship (SAR) studies. 5 key findings →
Evidence: low
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Concentrations of CSF APP were significantly lower in T- compared to T+ individuals across all clinical diagnostic groups across cohorts, regardless of A± status (Figure 1). 5 key findings →
Participants: 384 Evidence: low
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We sequenced a total of 38,577 nuclei and detected an average of 2,700 genes per cell. 5 key findings →
Participants: 38,577 Evidence: low
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We observed two promising biomarkers of AD, mLOY and APR, both contribute discriminating AD and CI but differently. 5 key findings →
Participants: 30 Evidence: low
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For the 30 clinically-diagnosed DLB participants, 23 (77%) were SAA-positive. 5 key findings →
Design: longitudinal study Evidence: moderate
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Biomarkers specific to AD pathology (p-tau217, GFAP) rather than peripheral inflammation had robust prognostic value in established AD. 5 key findings →
Participants: 333 Evidence: low
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The first search utilized the following MeSH terms and keywords: ‘Plasma Exchange’, ‘Plasmapheresis’, ‘Therapeutic plasma exchange’, ‘Apheresis’, ‘Aβ’, ‘p-tau’, ‘Total-tau’, ‘Alzheimer's disease’, ‘Cognitive dysfunction’, ‘neurodegenerative diseases’, ‘centrifugation’, ‘membranous’, and ‘filtration’ in the Title/Abstract, yielding 146 results. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to develop a conversion table for the Japanese version of the Montreal Cognitive Assessment (MoCA-J) to the Japanese version of the Mini-Mental State Examination (MMSE-J) to facilitate prediction of the MMSE-J score from the MoCA-J score. 1 key finding →
Participants: 121 Evidence: low
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The observation group had significantly higher blood uric acid levels than the control group (P<0.05). 5 key findings →
Participants: 84 Evidence: low
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Our findings may contribute to the growing body of knowledge on the vascular contributions to cognitive function and may help identify potential biomarkers for the early detection and intervention of AD. 4 key findings →
Design: cross-sectional Evidence: moderate
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In a cohort of 75 patients who completed Moneta's program (average age 73 ± 10, average MoCA score 20 ± 5), 59% had MCI and 33% had dementia. 5 key findings →
Participants: 75 Evidence: moderate
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value = 0.04). ε4 on cognition is mediated by structural brain imaging markers, driven mainly by cerebral microbleeds. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
OSA components are positively associated with the risk of ADRD. 5 key findings →
Participants: 14 Evidence: low
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The spontaneous self-assembly of proteins and nucleic acids into biomolecular condensates has been shown to ubiquitously contribute to the functional compartmentalization of the cell. 1 key finding →
Evidence: low
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The coronavirus disease 2019 (COVID-19) pandemic has been linked to long-term neurological effects with multifaceted complications of neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several reports confirmed possible inadvertent iatrogenic intracranial transmission of Aβ pathology via medical and surgical procedures (1,2).A common molecular mechanism, described in prion diseases, is proposed to trigger the replication and spread of different misfolded proteins in the central nervous system (CNS), causing different neurodegenerative diseases associated with disease-specific proteins such as α-synuclein in Parkinson's disease, and amyloid-beta (Aβ) in Alzheimer's disease, and cerebral amyloid angiopathy (CAA) (3). 5 key findings →
Participants: 125 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.
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 →