27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
PIB-positive subjects with mild cognitive impairment (MCI) are significantly more likely to convert to AD than PIB-negative patients, faster converters having higher PIB retention levels at baseline than slower converters. 4 key findings →
Evidence: low
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Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD. 2 key findings →
Design: cross-sectional Evidence: moderate
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The proportion of progressors was 11% (8/41), 34% (14/41), 56% (19/34), and 71% (60/85) in A-N-, A+N-, SNAP, and A+N+, respectively; the proportion of APOE ε4 carriers was 29%, 70%, 31%, and 71%, respectively, with the SNAP group featuring a significantly different proportion than both A+N- and A+N+ groups (p ≤ 0.005). 2 key findings →
Participants: 201 Evidence: low
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Participants age 60-85 years deemed cognitively unimpaired were disclosed an elevated or not elevated brain amyloid result by a certified clinician. 5 key findings →
Participants: 3,686 Evidence: high
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Butylphthalide may restore abnormal organization in structural networks of patients with MCI due to AD, and baseline network metrics could be predictive markers for therapeutic efficacy of butylphthalide. 4 key findings →
Participants: 270 Evidence: low
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The results indicate that incorporating MI can positively influence cognitive status, emotional status, and the quality of life in older adults diagnosed with early-stage dementia. 4 key findings →
Design: randomized controlled trial Participants: 55 Evidence: high
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Neuropsychiatric symptoms (NPS) are common in dementia and in predementia syndromes such as mild cognitive impairment (MCI). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MBI may be an earlier marker of neurodegenerative disease than MCI, captured at the stage of subjective cognitive decline or before, raising the possibility that MBI represents a novel target for dementia clinical trials or prevention strategies. 3 key findings →
Participants: 9,931 Evidence: low
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Modifiable risk factors for MCI should be sought (at the very latest) in persons who already have MCI, as their optimal treatment may improve these patients' cognitive performance or keep the existing deficits from progressing. 4 key findings →
Evidence: low
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Patients with MCI had a predominant memory impairment with relative sparing of other cognitive domains and were intermediate between clinically normal individuals and patients with AD on cognitive and functional ratings. 3 key findings →
Participants: 769 Evidence: low
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The recent development of tau-specific positron emission tomography (PET) tracers enables in vivo quantification of regional tau pathology, one of the key lesions in Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Differences in white matter hyperintensities (WMH) associated with increasing cognitive impairment appear related to both extent and spatial location. 5 key findings →
Design: post-hoc analysis Participants: 26 Evidence: low
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Among patients with cognitive symptoms, larger choroid plexus volume was associated with severity of cognitive impairment in the Alzheimer disease spectrum. 5 key findings →
Participants: 532 Evidence: low
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Cerebral amyloid deposition is associated with APOE4 carrier status in older healthy control subjects and symptomatic AD patients, and increases with age in older cognitively normal individuals. 3 key findings →
Participants: 245 Evidence: low
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Our data suggest that interactions between biomarkers in AD result in a 2-phase phenomenon of pathological cortical thickening associated with low CSF Aβ, followed by atrophy once CSF p-tau becomes abnormal. 3 key findings →
Design: cross-sectional Participants: 145 Evidence: low
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Using the OSHPE criteria, we found more participants with MCI than with frailty. 4 key findings →
Design: cross-sectional Participants: 5,104 Evidence: low
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Alzheimer's Disease is a complex, multifactorial, and comorbid condition. 1 key finding →
Design: longitudinal study Evidence: moderate
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The results demonstrated that CCIs have beneficial effects on domain-specific cognition in people with MCI but no significant effects on people with dementia. 5 key findings →
Design: systematic review Evidence: high
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Despite general agreement about the boundaries of Alzheimer disease (AD), establishing a maximum limit for Alzheimer-type pathology in cognitively intact individuals might aid in defining more precisely the point at which Alzheimer pathology becomes clinically relevant. 1 key finding →
Participants: 19 Evidence: low
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Metabolomics identified key disease-related metabolic changes and disease-progression-related changes. 1 key finding →
Evidence: low
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Neuroimaging has made it possible to measure pathological brain changes associated with Alzheimer's disease (AD) in vivo. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that the initial 1H MRS change in the pathologic progression of AD is an increase in MI/Cr. 4 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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Alzheimer's disease (AD) is a progressive and irreversible brain degenerative disorder. 2 key findings →
Evidence: low
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Intimate metabolic host-microbiome crosstalk regulates immune, metabolic, and neuronal response in health and disease, yet remains untapped for biomarkers or intervention for disease. 2 key findings →
Participants: 77 Evidence: moderate
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From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 →