28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The construct of mild cognitive impairment (MCI) has been proposed to identify patients at risk of developing Alzheimer's disease (AD) in the pre-clinical stage. 3 key findings →
Evidence: low
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There are many factors that strongly influence the aetiology, development, and progression of cognitive decline in old age, mild cognitive impairment (MCI), and Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Nerve growth factor (NGF)-dependent cholinergic basal forebrain neurons degenerate during the progression of Alzheimer disease (AD). 2 key findings →
Evidence: low
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The delayed recall of auditory verbal learning test (AVLT_DR) identified 116 subjects as MCI, resulted in the conversion rate as 44% over the roughly 30-month time interval, missed 7.8% incipient Alzheimer's disease (AD) patients in SCD group who eventually converted to dementia. 3 key findings →
Participants: 95 Evidence: low
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No disease-modifying therapy is currently available for Alzheimer's disease, but therapies are in development, and one may become available in the near future. 1 key finding →
Evidence: low
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Mild cognitive impairment (MCI) describes a state of cognitive functioning that is below defined norms, yet falls short of dementia in severity. 1 key finding →
Evidence: low
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Several studies have recently shown that basal ganglia (BG) deterioration leads to distinctive impairments in the domains of syntax, action verbs, and action semantics. 3 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive decline in multiple cognitive domains. 2 key findings →
Evidence: low
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Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. 4 key findings →
Evidence: low
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Impairment in instrumental activities of daily living (IADL) heralds the transition from mild cognitive impairment (MCI) to dementia and is a major source of burden for both the patient and caregiver. 4 key findings →
Evidence: low
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Apolipoprotein E ε4 (APOE ε4) bring the higher risk of Alzheimer' Disease (AD). 4 key findings →
Participants: 1,610 Evidence: low
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Subtle changes in objective spatial navigation ability have been observed in the preclinical stage of Alzheimer disease (AD) cross-sectionally and have been found to predict clinical progression. 4 key findings →
Design: longitudinal study Evidence: moderate
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Plasma glial fibrillary acidic protein (GFAP) has emerged as a promising biomarker of astrocytic reactivity in preclinical Alzheimer´s Disease (AD). 4 key findings →
Participants: 143 Evidence: low
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In this study we investigated impaired awareness of cognitive deficits in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). 4 key findings →
Evidence: low
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We investigated possible abnormalities in the retinal nerve fiber layer (RNFL) and macula lutea of patients diagnosed with Alzheimer's disease (AD) and mild cognitive impairment (MCI) and tested for any correlation with the severity of dementia. 4 key findings →
Participants: 72 Evidence: low
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Mild Cognitive Impairment (MCI) is a transitional stage between normal aging and dementia and people with MCI are at high risk of progression to dementia. 4 key findings →
Evidence: low
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Fourteen participants (21.5%) converted to MCI, and 24 (36.9%) were classified as Prog-1.Plasma biomarkers did not show consistent predictive performance across predefined endpoints (all p>0.05), although NfL demonstrated modest discrimination for MCI conversion (area under the curve [AUC] 0.686, p=0.008).Hippocampal volume demonstrated significant discriminative performance for MCI conversion (AUC 0.765, p=0.016) and Prog-1 (AUC 0.933, p<0.001).For Prog-2, hippocampal volume showed high discrimination (AUC 0.952, p<0.001).WMH grade also demonstrated significant discrimination for MCI conversion (AUC 0.835, p<0.001) and Prog-1 (AUC 0.857, p<0.001).Bootstrap analyses (1,000 iterations) tended to show higher AUC estimates for imaging markers compared with plasma biomarkers. 2 key findings →
Evidence: moderate
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<0.001), with key domain correlations ≥0.7 (language, memory, executive). 5 key findings →
Design: cross-sectional Participants: 639 Evidence: moderate
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Cognitive decline is a condition affecting almost one sixth of the elder population and is widely regarded as one of the first manifestations of Alzheimer's disease. 2 key findings →
Participants: 145 Evidence: moderate
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Predicting the transition from mild cognitive impairment (MCI) to Alzheimer's disease (AD) has important clinical significance for dementia prevention and improving patient prognosis. 4 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is an early stage of non-age-related cognitive decline with an increased risk of progressing to dementia. 4 key findings →
Evidence: low
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Mild cognitive impairment (MCI) represents a transitional stage between normal aging and dementia, often considered critical for dementia prevention. 1 key finding →
Evidence: low
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At baseline, SCDp were older, had a higher prevalence of hypertension and hypercholesterolemia and had worst performance on tests related to processing speed, verbal fluency, visual memory, verbal memory, and executive functioning. 4 key findings →
Participants: 450 Evidence: low
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Alzheimer's disease (AD) is a complex, progressive, and irreversible neurodegenerative disorder marked by cognitive decline and memory loss. 1 key finding →
Evidence: low
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10 of the 2,188 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →