27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Increasing numbers of people are developing type 2 diabetes mellitus, but interventions to prevent and treat the classic microvascular and macrovascular complications have improved, so that people are living longer with the condition. 2 key findings →
Evidence: high
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Macrophages are central orchestrators of the tissue response to injury, with distinct macrophage activation states playing key roles in fibrosis progression and resolution. 4 key findings →
Evidence: low
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Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear. 4 key findings →
Evidence: low
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In linear mixed models, vascular endothelial growth factor was significantly associated with incident DWI-positive lesions over 1 year. 5 key findings →
Design: cross-sectional Participants: 181 Evidence: moderate
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Florbetaben PET shows high sensitivity and specificity for the detection of histopathology-confirmed neuritic β-amyloid plaques and may thus be a valuable adjunct to clinical diagnosis, particularly for the exclusion of AD.
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Increased awareness of cognitive and behavioural change in amyotrophic lateral sclerosis has been driven by various clinic-based and population-based studies. 5 key findings →
Evidence: low
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AD is a neurodegenerative disease, and its frequency is often reported to be higher for women than men: almost two-thirds of patients with AD are women. 4 key findings →
Evidence: low
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FDG-PET was performed on a cohort of 79 patients with newly diagnosed PD (mean disease duration 8 months) and 20 unrelated controls. 4 key findings →
Participants: 79 Evidence: moderate
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The symptoms of Alzheimer disease reflect a loss of neural circuit integrity in the brain, but neurons do not work in isolation. 2 key findings →
Evidence: low
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Cardiovascular disease (CVD) is the leading cause of mortality globally, with over 20 million deaths each year. 1 key finding →
Evidence: low
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Accelerated atrophy of medial temporal lobe subregions was evident already during preclinical AD. 5 key findings →
Participants: 363 Evidence: low
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia with no specific treatment, of which molecular mechanisms remain poorly understood. 2 key findings →
Participants: 40,000 Evidence: low
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Healthcare costs are already elevated in early subjective and objective cognitive impairment, driven by formal and informal care. 5 key findings →
Design: cross-sectional Evidence: moderate
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Machine learning does not differentiate clinically relevant disease categories yet. 2 key findings →
Evidence: low
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Glial proliferation and activation are associated with disease progression in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia. 2 key findings →
Evidence: low
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Rare variants in TREM2 cause susceptibility to late-onset Alzheimer's disease. 4 key findings →
Evidence: low
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Our understanding of the functional heterogeneity of resident versus recruited macrophages in the diseased liver is limited. 4 key findings →
Evidence: low
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The apolipoprotein E (APOE)ε4 allele is the strongest genetic risk factor for late-onset AD and is associated with aberrant cerebrospinal fluid levels (CSF) of total tau (t-tau), phosphorylated tau (p-tau), and amyloid-β (Aβ). 4 key findings →
Design: cohort study Evidence: moderate
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Alzheimer's disease (AD) is the leading cause of dementia, characterized by the accumulation of amyloid-beta (Aβ) and neurofibrillary tangles. 4 key findings →
Participants: 16 Evidence: low
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White matter hyperintensities (WMH) are among the most common radiological abnormalities in the ageing population and an established risk factor for stroke and dementia. 4 key findings →
Evidence: low
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Microglia are implicated in the progression of Alzheimer's disease (AD) pathology from its earliest stages, suggesting that cerebrospinal fluid (CSF) microglia profiling across clinical AD stages can aid in treatment development and monitoring. 3 key findings →
Participants: 834 Evidence: low
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A total of 44 experts participated in 3 survey rounds, with 28 to 31 participants each. 5 key findings →
Participants: 31 Evidence: low
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Early and accurate detection of Alzheimer's disease (AD) is essential for timely intervention and development of disease-modifying treatments. 1 key finding →
Design: longitudinal study Evidence: moderate
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Though results of pivotal studies in early (prodromal/mild) Alzheimer's disease are awaited, results to date in more established (mild to moderate) Alzheimer's disease have been equivocal and no disease modifying agents are either licensed or can be currently recommended for clinical use. 1 key finding →
Evidence: high
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Cerebral small vessel disease (CSVD) is a very common neurological disease in older people. 4 key findings →
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. 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 →