27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau is a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neurons of the cholinergic basal forebrain (CBF) in Alzheimer's disease (AD). 3 key findings →
Evidence: low
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To clarify the involvement of the posterior cingulate cortex (PCC) in Alzheimer's disease (AD), we analyzed brain volume loss by voxel-based morphometry. 4 key findings →
Participants: 20 Evidence: low
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AD is characterised by a significant alteration in the circulating levels of the cytokines and receptors of the IL-1 family. 5 key findings →
Evidence: low
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Amyloid imaging represents a major advance in neuroscience, enabling the detection and quantification of pathologic protein aggregations in the brain. 5 key findings →
Evidence: low
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We found a general trend of increased degree of asymmetry with increasing severity of diagnosis. 5 key findings →
Evidence: low
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Although the two pathological hallmarks of Alzheimer's disease (AD), senile plaques composed of amyloid-β (Aβ) peptides and neurofibrillary tangles (NFTs) consisting of hyperphosphorylated tau, have been studied extensively in postmortem AD and relevant animal and cellular models, the pathogenesis of AD remains unknown, particularly in the early stages of the disease where therapies presumably would be most effective. 2 key findings →
Evidence: low
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Poor subjective sleep quality is linked to reduced brain volume and cortical thickness (CTh), but associations with objective sleep measures, particularly regarding sex and AD pathology, remain unclear. 4 key findings →
Evidence: low
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Although preclinical dementia is characterized by decline in cognition and daily functioning, little is known on their temporal sequence. 4 key findings →
Evidence: low
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Mild cognitive impairment (MCI) has been considered a transitional state between normal aging and dementia, characterised by memory impairment but normal general cognitive functioning. 4 key findings →
Evidence: low
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Four cognitive phenotypes emerged. One phenotype (18% of Aβ+ participants) showed the steepest cognitive decline, highest progression on the CDR, greater baseline medial temporal tau, and fastest neocortical tau accumulation over 4.6 years (hazard ratio [HR] for decline ≈ 2.9). 3 key findings →
Design: longitudinal study Evidence: moderate
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Lifestyle factors and ambient air pollution are linked to dementia and CMDs, yet few studies have investigated their impact on dementia risk in CMDs patients at the same time. 1 key finding →
Participants: 438,681 Evidence: low
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The three cognitive assessment tools were valid for detecting subjects with MCI or dementia according to ROC analysis. 5 key findings →
Design: cross-sectional Participants: 1,090 Evidence: low
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Alzheimer's disease (AD) is marked by progressive cognitive decline, highlighting the importance of cognitive assessment in both clinical practice and research. 1 key finding →
Participants: 1,447 Evidence: low
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These results provide clear evidence that CU older adults with both amyloid plaques and tau aggregates measured with PET will develop cognitive impairments if the disease is not stopped. 2 key findings →
Design: cohort study Evidence: moderate
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From 356 participants, 104 were MCI-C, whereas 252 were MCI-NC. 5 key findings →
Participants: 356 Evidence: low
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The Level 3 model achieved high classification performance (AUC: 93.98%), and the Level 1 model achieved comparable performance (AUC: 91.53%). 5 key findings →
Participants: 31,081 Evidence: low
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During a 7-year median follow-up, type 2 diabetes was associated with the highest risk of all-cause dementia (hazard ratio [HR] 1.18, 95% confidence interval [CI]: 1.06 to 1.31), followed by hypertension and hyperlipidemia. 5 key findings →
Evidence: moderate
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Alzheimer's disease (AD) develops over a prolonged asymptomatic phase marked by silent pathology. 1 key finding →
Participants: 102 Evidence: low
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Dementia developed in 104 individuals (29.6%), including 85 (22.4%) who met core clinical criteria for probable and possible Alzheimer's disease dementia. 3 key findings →
Participants: 398 Evidence: low
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The results indicated that residence location, alcohol consumption, life satisfaction, depressive symptoms, and education level are key factors influencing the risk of MCI among older adults with functional disability. 3 key findings →
Design: longitudinal study Evidence: moderate
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BackgroundPatients with dementia face driving difficulties and, at some point, cease driving. 2 key findings →
Design: longitudinal study Evidence: moderate
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Diabetes is a significant modifiable risk factor for cognitive dysfunction. 1 key finding →
Design: open-label trial Participants: 396 Evidence: high
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Alzheimer’s disease (AD) presents a significant global health challenge, necessitating accurate and early prediction methods for effective intervention and treatment planning. 3 key findings →
Design: longitudinal study Evidence: moderate
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During follow-up 20 SCD and 99 MCI patients developed dementia. 5 key findings →
Participants: 184 Evidence: moderate
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Elevated BMI/BV associated with lower BBM concentrations, especially for p-Tau217 and NfL, independent of brain amyloid burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,141 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →