27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
c GMP , and not c AMP levels, were significantly lower in the CSF of patients diagnosed with mild AD when compared with nondemented controls. 5 key findings →
Participants: 79 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Over the past several years, experiments with synthetic amyloid-beta peptide (Abeta) and animal models have strongly suggested that pathogenesis of Alzheimer's disease (AD) involves soluble assemblies of Abeta peptides (Trends Neurosci. 24 (2001) 219). 1 key finding →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and synapse loss. 2 key findings →
Evidence: low
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Oxidative damage is a feature of many age-related neurodegenerative diseases, including Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of the free radical-mediated lipid peroxidation of unsaturated lipids, particularly arachidonic acid, in cellular membranes. 2 key findings →
Evidence: low
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The role of hypoperfusion in Alzheimer's disease (AD) is a vital component to understanding the pathogenesis of this disease. 3 key findings →
Evidence: low
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Increasing evidence supports a role for oxidative damage in the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI), the earliest clinically detectable phase of the trajectory toward dementia and Alzheimer's disease (AD), led to the need for even earlier detection and prevention of AD. 2 key findings →
Evidence: low
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Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive impairment (MCI) and late-stage Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Mild cognitive impairment refers to the transitional state between the cognitive changes of normal aging and the fully developed clinical features of dementia. 5 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is considered to be an early stage in the progression of Alzheimer's disease (AD) providing an opportunity to investigate brain pathogenesis prior to the onset of dementia. 5 key findings →
Evidence: low
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There is a great interest in the relationship between Mild Cognitive Impairment (MCI) and the progression to Alzheimer's disease (AD). 2 key findings →
Participants: 34 Evidence: low
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As different signature changes associated with particular stages of disease burden are identified and validated, we anticipate expanded application of qEEG as a reliable and sensitive biomarker(s) of MCI and early Alzheimer's disease. 2 key findings →
Evidence: low
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Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Advances in AD biomarker research have demonstrated changes in amyloid-beta (Aβ), brain metabolism and other pathophysiologies prior to the onset of memory loss, with some markers possibly changing one or two decades earlier. 3 key findings →
Evidence: low
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The clinical hallmark of Alzheimer's disease (AD) is a gradual decline in cognitive function. 1 key finding →
Evidence: low
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Synaptic integrity is now recognized as a central component of Alzheimer's disease. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia and mitigating amyloid-β (Aβ) levels may serve as a rational therapeutic avenue to slow AD progression. 5 key findings →
Evidence: low
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Researchers have begun to characterize the subtle biological and cognitive processes that precede the clinical onset of Alzheimer disease (AD), and to set the stage for accelerated evaluation of experimental treatments to delay the onset, reduce the risk of, or completely prevent clinical decline. 4 key findings →
Evidence: low
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The findings from this study add to the anatomical knowledge of hippocampal subregions in PD, allowing us to understand the unique functional contribution of each subfield. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is characterized by the pathological accumulation of amyloid plaques and hyperphosphorylated tau proteins, leading to disruptions in synaptic transmission and neural circuit alterations. 4 key findings →
Evidence: low
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Statistical analysis revealed a trend toward more impaired prefrontal FC with declining cognitive function. 5 key findings →
Evidence: low
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The paper discusses according to prevailing diagnostic systems and algorithms, which cognitive domains that are relevant to investigate, which tests that may be relevant, what kind of norms have satisfactory quality, which cut-off scores do best balance sensitivity and specificity in a neurodiagnostic context, and what kind of conclusions and recommendations that can be drawn from neuropsychological findings. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the CN group, cerebral microbleed (CMB) progression was associated with the decline in language function (p < 0.05), and deep white matter hyperintensity (WMH) progression was associated with a decline in memory function (p < 0.05). 4 key findings →
Design: longitudinal study Participants: 432 Evidence: moderate
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Mild cognitive impairment (MCI) is an early stage in the progression toward dementia. 1 key finding →
Design: longitudinal study Evidence: moderate
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< 0.0001) were significantly higher for the MCI cohort. 3 key findings →
Design: cohort study 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 →