27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The aim of this study was to explore concentrations differences of soluble amyloid precursor protein (sAPP) α and β in blood plasma in patients with probable Alzheimer's disease (AD) and cognitively healthy age-matched control subjects, as well as patients with behavioural variant frontotemporal dementia (bvFTD). 2 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with aMCI who had epilepsy presented with symptoms of cognitive decline 6.8 years earlier than patients with aMCI who did not have epilepsy (64.3 vs 71.1 years; P = .02). 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast, all Alzheimer's disease variants showed diffuse patterns of (11)C-labelled Pittsburgh compound B binding, with posterior cortical atrophy additionally showing elevated uptake in occipital cortex compared with early-onset Alzheimer's disease. 4 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
The predictive value of Aβ42 was highly affected by the type of collection tube used. 5 key findings →
Participants: 1,966 Evidence: low
Full summary, score breakdown and related studies → Original source
Genome-wide association studies have identified a number of risk variants for Alzheimer’s disease implicated in inflammatory responses (Bettens et al., 2013); exome sequencing has revealed polymorphisms in the microglial receptor TREM2 gene as a rare but significant risk for Alzheimer’s disease (Guerreiro et al., 2013; Jonsson et al., 2013); and recently, the CD33 risk allele has been shown to inhibit microglial clearance of amyloid-β (Bradshaw et al., 2013; Griciuc et al., 2013). 5 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
As life expectancy lengthens, dementia is becoming a significant human condition in terms of its prevalence and cost to society worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The prevention of Alzheimer's disease (AD) has become a real challenge due to its rising prevalence and the lack of an effective cure. 3 key findings →
Evidence: high
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Although age remains the main risk factor to suffer Alzheimer's disease (AD) and vascular dementia (VD), type 2 diabetes (T2D) has turned up as a relevant risk factor for dementia. 2 key findings →
Evidence: low
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The structural brain network of patients showed reduced local efficiency compared to controls. 2 key findings →
Evidence: low
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Symptoms revealed as "most problematic" varied by measurement criterion. 4 key findings →
Participants: 177 Evidence: low
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These results suggest that mechanisms leading to atherosclerosis might also lead to an increased number of perivascular spaces. 5 key findings →
Participants: 706 Evidence: low
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Maintenance of brain function depends on a constant blood supply. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Obesity significantly increases the risk of developing type 2 diabetes, hypertension, coronary heart disease, stroke, fatty liver disease, dementia, obstructive sleep apnea and several types of cancer. 1 key finding →
Evidence: low
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There is a great deal of evidence suggesting an important role for systemic inflammation in the pathogenesis of Alzheimer's disease. 1 key finding →
Evidence: low
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The salience network (SN) serves to identify salient stimuli and to switch between the central executive network (CEN) and the default-mode network (DMN), both of which are impaired in Alzheimer's disease (AD)/amnestic mild cognitive impairment (aMCI). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Soluble oligomers of the amyloid-β (Aβ) peptide cause neurotoxicity, synaptic dysfunction, and memory impairments that underlie Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Therapies designed to decrease the level of SOD1 are currently in a clinical trial for patients with superoxide dismutase (SOD1)-linked familial amyotrophic lateral sclerosis (ALS). 4 key findings →
Evidence: low
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Frailty is commonly considered as a syndrome with several symptoms, including weight loss, exhaustion, weakness, slow walking speed and physical inactivity. 4 key findings →
Participants: 654 Evidence: low
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Traumatic brain injury (TBI) in early to mid-life is associated with an increased risk of dementia in late life. 4 key findings →
Participants: 62 Evidence: low
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Neuropsychiatric symptoms are prevalent in mild cognitive impairment (MCI) and Alzheimer disease (AD) and commonly measured using the Neuropsychiatric Inventory (NPI). 4 key findings →
Design: cross-sectional Evidence: low
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Mutations in the TAR DNA Binding Protein gene (TARDBP), encoding the protein TDP-43, were identified in amyotrophic lateral sclerosis (ALS) patients. 4 key findings →
Evidence: low
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The specific CB2 cannabinoid receptor agonist JWH-133 induced cognitive improvement in double AβPP/PS1 transgenic mice, a genetic model of Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
When using ethnic group-specific norms, NP and functional abilities predicted diagnosis in both groups with no significant differences but BPS was only significant in Hispanics. 5 key findings →
Participants: 444 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Astrocytosis shows a distinct regional pattern in AD brain compared to fibrillar Aβ, suggesting that different types of astrocytes may be associated with the pathophysiological processes in AD. 3 key findings →
Evidence: low
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 →