27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
= 62.87, SD = 9.46, 36.52% female). Both networks were densely connected, reflecting comorbidity between neuropsychiatric symptoms and cognitive scores. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild Cognitive Impairment (MCI) is a transitional stage between normal age-related cognitive decline and the more severe cognitive loss seen in dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
At baseline, the mean ZBI score was 24.5 ± 15.2 and correlated positively with caregiver CES-D and STAI scores and with patient neuropsychiatric symptoms (NPI-frequency × severity) and distress felt by the caregiver (NPI-distress). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI) and sarcopenia are prevalent age-related conditions that often coexist and share common mechanisms such as chronic inflammation, reduced neuroplasticity, and impaired muscle function. 1 key finding →
Design: narrative review Evidence: low
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The results of the data analysis revealed two main categories: emotional schemas in mild cognitive impairment and understanding the meaning of the diagnosis. 5 key findings →
Participants: 16 Evidence: low
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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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Overall, both machine learning techniques had an equivalent performance. 4 key findings →
Evidence: low
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These findings highlight hippocampal atrophy as a key pathway linking Aβ burden to cognitive impairment. 4 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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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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Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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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The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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. 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 27,380 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 →