27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
There is accumulating evidence that soluble amyloid-beta (Abeta) oligomers, rather than amyloid fibrils, are the principal pathogenic species in Alzheimer disease (AD). 4 key findings →
Participants: 25 Evidence: low
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Nerve growth factor (NGF) is critical for the regulation, differentiation, and survival of basal forebrain cholinergic neurons that degenerate in the late stage of Alzheimer disease (AD). 3 key findings →
Participants: 20 Evidence: low
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Alzheimer's disease (AD) not only involves loss of memory functions, but also prominent deterioration of sleep physiology, which is already evident at the stage of mild cognitive impairment (MCI). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD. 3 key findings →
Evidence: low
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The results indicate that a-MCI and na-MCI display a stable pattern of deficits to attention, working memory, and executive function. 3 key findings →
Design: longitudinal study Evidence: moderate
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We believe this to be the first demonstration of myelin loss in MCI, Alzheimer's disease, and vascular dementia using a method that provides a quantitative magnetic resonance imaging-based measure of myelin. 2 key findings →
Evidence: low
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Alzheimer's disease (AD) is a devastating disorder of increasing prevalence in modern society. 2 key findings →
Participants: 86 Evidence: low
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TP42/40 demonstrated value in the identification of individuals suffering a-MCI, in the prediction of progression to dementia, and in the detection of underlying AD pathology revealed by FDG-PET, Amyloid-PET and CSF biomarkers, being, thus, consistently associated with all the well-established indicators of AD. 3 key findings →
Participants: 145 Evidence: low
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From 348 patients, 126 evolved to dementia (36.2%). 2 key findings →
Participants: 348 Evidence: low
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Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although Alzheimer's disease (AD) is primarily a neurocognitive disorder, it also results in prominent neuropsychiatric symptoms (NPS). 2 key findings →
Evidence: low
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Seventy-five subjects with MCI progressed to dementia by last follow-up. 2 key findings →
Evidence: low
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Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Identifying pre-clinical Alzheimer's disease (AD) in subjects with mild cognitive impairment (MCI) is a major issue in clinical diagnosis. 5 key findings →
Evidence: low
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Our novel neuropsychological approach improved the staging of MCI by (1) capturing individuals at an early symptomatic stage, (2) minimizing false-positive cases, and (3) identifying a late MCI group further along the disease trajectory. 2 key findings →
Evidence: low
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The combination of neuropsychological tests and P300 measurements proved useful in improving reliability and increasing sensitivity to early cognitive decline or disease progression in AD patients. 3 key findings →
Design: longitudinal study Evidence: moderate
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Thirty patients with MCI and nonpathologic CSF total tau levels, nine patients with MCI and pathologic CSF total tau levels, and 16 age-matched healthy control subjects underwent diffusion-tensor imaging at baseline and after a mean follow-up of 2.6 years ± 0.54 (standard deviation), with range of 1.58-3.98 years. 4 key findings →
Design: longitudinal study Evidence: moderate
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Our purpose was to characterize a state of mild cognitive impairment (MCI) in Parkinson's disease (PD) (PD-MCI) that would be analogous to the MCI that is posited as a precursor of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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All versions of the Montreal Cognitive Assessment (MoCA) lack population-based data of 80-plus individuals. 4 key findings →
Design: cross-sectional Evidence: low
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The AB Cognitive Screen (ABCS) 135, sensitive in differentiating MCI from dementia, was modified to improve sensitivity and specificity, producing the quick mild cognitive impairment (Qmci) screen. 4 key findings →
Participants: 630 Evidence: low
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Plasma neurofilament light (NFL) levels may be a marker of neuronal injury. 4 key findings →
Participants: 193 Evidence: low
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Late-life depression (LLD) is associated with development of different types of dementia. 4 key findings →
Participants: 185 Evidence: low
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Alzheimer's Disease (AD), one of the main causes of death in elderly people, is characterized by Mild Cognitive Impairment (MCI) at prodromal stage. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is characterised by a dynamic process of neurocognitive changes from normal cognition to mild cognitive impairment (MCI) and progression to dementia. 4 key findings →
Evidence: moderate
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A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →
Design: cross-sectional Evidence: low
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 →