Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Late Onset Alzheimer's disease (LOAD) is the leading cause of dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The identification of biological and pathophysiological processes implicated in different forms of dementia is itself dependent on reliable descriptions of cognitive performance and capacities. 2 key findings →
Participants: 60 Evidence: moderate
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Tar DNA Binding Protein-43 (TDP-43) is a principle component of inclusions in many cases of frontotemporal lobar degeneration (FTLD-U) and amyotrophic lateral sclerosis (ALS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The discovery and reliable detection of markers for neurodegenerative diseases have been complicated by the inaccessibility of the diseased tissue--such as the inability to biopsy or test tissue from the central nervous system directly. 2 key findings →
Participants: 69 Evidence: low
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We developed an accurate prognostic model for predicting MCI-to-dementia progression over a three-year period. 4 key findings →
Participants: 139 Evidence: low
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Dehydration can affect the volume of brain structures, which might imply a confound in volumetric and morphometric studies of normal or diseased brain. 3 key findings →
Design: longitudinal study Evidence: moderate
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Among 1,528,885 adults with type 2 diabetes (mean age, 58 years; 49.2% women), GLP-1 receptor agonists plus metformin were associated with lower incidence of vascular dementia (HR, 0.46; 95% CI, 0.37-0.57), mild cognitive disorder (HR, 0.79; 95% CI, 0.66-0.95), and Alzheimer disease (HR, 0.46; 95% CI, 0.31-0.70). 5 key findings →
Design: cohort study Participants: 1,528,885 Evidence: moderate
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Alzheimer's Disease (AD) currently affects more than 5 million Americans, with numbers expected to grow dramatically as the population ages. 4 key findings →
Evidence: low
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Glial fibrillary acidic protein (GFAP) is the main astrocytic intermediate filament (IF). 1 key finding →
Evidence: low
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Detecting early morphological changes in the brain and making early diagnosis are important for Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Our objective was to determine whether the consumption of green tea, coffee, or black tea influences the incidence of dementia and mild cognitive impairment (MCI) in older people. 3 key findings →
Participants: 723 Evidence: low
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According to the World Health Organization (WHO), dementia is the seventh leading reason of death among all illnesses and one of the leading causes of disability among the world's elderly people. 1 key finding →
Evidence: low
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Fibroblast growth factor 23 is an emerging vascular biomarker, recently associated with cerebral small vessel disease and poor cognition in patients on dialysis. 4 key findings →
Evidence: moderate
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Late onset Alzheimer's disease (LOAD) etiology is influenced by complex interactions between genetic and environmental risk factors. 4 key findings →
Evidence: low
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This study demonstrated the use of speech measures in the identification of those with an oral-motor deficit, and showed the usefulness of performing a relatively simple reading test to assess speech versus pause behaviors across the ALS-FTD disease continuum. 3 key findings →
Participants: 136 Evidence: low
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Diffusion tensor imaging (DTI) based assessment of white matter fiber tract integrity can support the diagnosis of Alzheimer's disease (AD). 4 key findings →
Participants: 137 Evidence: low
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Autophagy is an intracellular degradation pathway that functions in protein and organelle turnover in response to starvation and cellular stress. 4 key findings →
Evidence: low
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Microglial cells closely interact with senile plaques in Alzheimer's disease and acquire the morphological appearance of an activated phenotype. 4 key findings →
Evidence: low
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Using a targeted proteomic screen, we identified novel candidate biomarkers that complement the best current CSF biomarkers for distinguishing very mildly/mildly demented from cognitively normal individuals. 5 key findings →
Evidence: low
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The pattern of regional decreased cortical thickness that relates to cognitive deterioration is present in PD-MCI patients, involving areas that play a central role in the storage of prior experiences, integration of external perceptions, and semantic processing. 2 key findings →
Participants: 26 Evidence: low
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In recent years, several high-dimensional, accurate, and effective classification methods have been proposed for the automatic discrimination of the subject between Alzheimer's disease (AD) or its prodromal phase {i.e., mild cognitive impairment (MCI)} and healthy control (HC) persons based on T1-weighted structural magnetic resonance imaging (sMRI). 4 key findings →
Participants: 326 Evidence: low
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Mild cognitive impairment (MCI) is a significant and increasingly recognized problem in individuals with type 2 diabetes mellitus (T2DM). 2 key findings →
Design: prospective cohort Participants: 100 Evidence: moderate
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We aim to clarify the mechanisms of acupuncture in treating mild cognitive impairment (MCI) and Alzheimer disease (AD) by using functional magnetic resonance imaging (fMRI). 3 key findings →
Evidence: low
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The aggregation of Aβ42-peptides and the formation of drusen in age-related macular degeneration (AMD) are due in part to the inability of homeostatic phagocytic mechanisms to clear self-aggregating Aβ42-peptides from the extracellular space. 4 key findings →
Evidence: low
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The optimized XGBoost model demonstrated superior performance, achieving an AUC of 0.85. 5 key findings →
Participants: 17,000 Evidence: low
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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.
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 →