28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The Australian Imaging, Biomarkers and Lifestyle (AIBL) study performed (11)C-Pittsburgh Compound B (PiB) scans in 177 healthy controls (HC), 57 mild cognitive impairment (MCI) subjects, and 53 mild Alzheimer's disease (AD) patients. 5 key findings →
Evidence: low
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In recent years, a series of publications have demonstrated a potentially important role for magnetic resonance imaging in the pre-mortem diagnosis of sporadic Creutzfeldt-Jakob disease. 1 key finding →
Evidence: low
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The strong correlation between hippocampal atrophy and beta-amyloid (Abeta) burden in the Pittsburgh compound B-positive healthy control group suggests that Abeta deposition in the inferior temporal neocortex is related to hippocampal synaptic and neuronal degeneration. 3 key findings →
Participants: 32 Evidence: low
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There has been recent interest in the application of machine learning techniques to neuroimaging-based diagnosis. 4 key findings →
Evidence: low
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The Alzheimer amyloid precursor protein (APP) is cleaved by several proteases, the most studied, but still unidentified ones, are those involved in the release of a fragment of APP, the amyloidogenic beta-protein A beta. 4 key findings →
Evidence: low
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White matter alterations are present in the majority of patients with Alzheimer's disease type dementia. 4 key findings →
Evidence: low
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The viral-inflammatory hypothesis of Alzheimer's disease offers a new paradigm, yet interventions like antivirals and vaccination present a paradox that challenge therapeutic development. 1 key finding →
Design: randomized controlled trial Evidence: high
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Genetic evidence strongly supports the view that Abeta amyloid production is central to the cause of Alzheimer's disease.
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When compared with the other groups, AD patients demonstrated significantly higher SUVRs (P Conclusion (18)F-florbetaben had high sensitivity for AD, clearly distinguished patients with FTLD from AD, and provided results comparable to those reported with (11)C-Pittsburgh Compound B in a variety of neurodegenerative diseases. 1 key finding →
Participants: 20 Evidence: low
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Recently, there has been growing interest in the glymphatic system (the functional waste clearance pathway for the central nervous system and its role in flushing solutes (such as amyloid ß and tau), metabolic, and other cellular waste products in the brain. 4 key findings →
Participants: 36 Evidence: moderate
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Of 1441 plasma proteins surveyed, a 12-protein signature significantly predicted cognitive decline (q-value < .05). 5 key findings →
Participants: 300 Evidence: moderate
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Our study demonstrated the robustness of a multisite Centiloid [ 11 C]PIB‐PET study and established a range of pathology‐based CL thresholds.
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The semantic and non-fluent/agrammatic variants are largely associated with frontotemporal lobar degeneration with TDP-43 and tau pathology, respectively. 3 key findings →
Evidence: low
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A location dynamics model and ADRD-focused future directions are offered for guiding rural practitioners, researchers, and policymakers in mitigating rural disparities. 1 key finding →
Evidence: low
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We performed hypothesis-free linkage analysis and exome sequencing in a family with two siblings who had neuronal ceroid lipofuscinosis (NCL). 3 key findings →
Evidence: low
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Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
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Population health research is increasingly focused on the genetic determinants of healthy ageing, but there is no public resource of whole genome sequences and phenotype data from healthy elderly individuals. 4 key findings →
Evidence: moderate
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Across imputed data sets, a median of 2,777 eligible individuals were included, with a median of 664 receiving a new HA prescription. 5 key findings →
Evidence: high
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Lifestyle behavioral change is a critical component for secondary prevention of stroke. 1 key finding →
Design: longitudinal study Evidence: high
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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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Plasma phosphorylated tau (p-tau)181, glial fibrillary acidic protein (GFAP), neurofilament light chain (NfL), and amyloid beta ratio (Aβ42/40) may have diagnostic and prognostic value in Alzheimer's disease (AD). 2 key findings →
Design: cross-sectional Participants: 1,298 Evidence: moderate
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Low CSF Aβ1-42 may be a significant predictor of POCD at 3 months. 5 key findings →
Participants: 59 Evidence: low
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Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. 3 key findings →
Participants: 588 Evidence: moderate
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The A(+)N(-) and A(+)N(+) groups had significantly faster cognitive decline than the A(-)N(-) group (0·08 SD per year for AIBL-Preclinical AD Cognitive Composite [PACC]; p Interpretation Brain amyloidosis, a surrogate marker of Alzheimer's disease pathology, is a risk factor for cognitive decline and for progression from preclinical stages to symptomatic stages of the disease, with neurodegeneration acting as a compounding factor. 2 key findings →
Evidence: low
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Alzheimer disease (AD) is the most common type of dementia, and is currently incurable; existing treatments for AD produce only a modest amelioration of symptoms. 1 key finding →
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 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 →