27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The most successful amyloid-targeting treatments achieve modest plaque reduction with marginal clinical benefit and significant adverse effects. 1 key finding →
Evidence: low
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The dominant research paradigm for Alzheimer's disease has focused on amyloid-beta plaqueremoval for over three decades, producing no curative therapy despite billions of dollars ofinvestment. 2 key findings →
Evidence: low
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Manganese-superoxide dismutase (Mn-SOD) was localized in the cerebral cortex and hippocampus of patients with Alzheimer-type senile dementia (ATD) by immunocytochemistry and the relationship of Mn-SOD with two major pathological features of ATD, i.e., senile plaques and neurofibrillar tangles (NFTs), was examined. 2 key findings →
Evidence: low
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Early hypoxic-ischemic brain lesions were examined regarding 26 autopsy cases which had severe asphyxia at birth and died within the first week. 1 key finding →
Evidence: low
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The research focuses on the use of biomarkers to diagnose Alzheimer’s disease (AD) in living individuals. 5 key findings →
Evidence: low
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Eine von 5 Frauen und einer von 10 Männern entwickeln eine Demenz vom Alzheimer-Typ, erläutern Palmqvist et al. zu Beginn ihrer Studie [1]. 5 key findings →
Evidence: low
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Als blutbasierter Biomarker zur Diagnose der Alzheimer-Krankheit gilt p-Tau217. 5 key findings →
Evidence: low
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Glial activation and neuroinflammation play significant roles in apoptosis as well as in the development of cognitive and memory deficits. 3 key findings →
Evidence: low
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INTRODUCTIONNovel capillary-blood collection methods have not yet been evaluated for a wide range of central nervous system (CNS) and neurodegenerative disease-related proteins. 2 key findings →
Evidence: low
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Alzheimers disease (AD) unfolds over decades preceding cognitive symptoms, and measuring the full scope of its molecular complexity remains difficult. 1 key finding →
Participants: 11,042 Evidence: low
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BACKGROUNDQuantitative amyloid-beta (A{beta})-PET is increasingly used in AD prevention trials. 3 key findings →
Design: longitudinal study Participants: 433 Evidence: moderate
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Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia. 5 key findings →
Evidence: low
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BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised. 1 key finding →
Evidence: low
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BackgroundEpidemiological studies increasingly associate several adult vaccinations with lower risk of Alzheimers disease (AD) and dementia, but the biological mechanisms underlying these observations remain unclear. 5 key findings →
Design: longitudinal study Participants: 192 Evidence: moderate
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Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →
Evidence: low
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BackgroundThe Centiloid (CL) scale standardizes global amyloid PET quantification and is widely used to define amyloid positivity. 5 key findings →
Design: meta-analysis Participants: 71 Evidence: high
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BackgroundFluid biomarkers enable the demonstration of the biological effects of novel therapies in Alzheimers disease (AD). 1 key finding →
Design: longitudinal study Participants: 65 Evidence: high
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INTRODUCTIONBiomarkers for monitoring disease activity and treatment response in peripheral neuropathies remain limited. 3 key findings →
Participants: 81 Evidence: low
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BackgroundPlasma phosphorylated tau at threonine 217 (p-Tau217) is a leading blood-based biomarker for Alzheimers disease (AD). 1 key finding →
Participants: 449 Evidence: moderate
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Service members with traumatic brain injury are at approximately two- to four-fold higher risk of Alzheimers disease or related dementias than those without such an injury, with risk increasing with injury severity. 5 key findings →
Participants: 57 Evidence: moderate
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INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations. 1 key finding →
Participants: 2,733 Evidence: low
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BackgroundThe 10 Year Health Plan for England indicates governmental intention to shift care from hospital to community. 1 key finding →
Evidence: low
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Plasma biomarkers of amyloid-associated tau phosphorylation (T1) and established tau proteinopathy (T2) can approximate Alzheimers disease stage, but whether plasma-defined stages correspond to broader biological states is unknown. 1 key finding →
Design: cross-sectional Participants: 1,035 Evidence: moderate
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--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up. 2 key findings →
Participants: 401 Evidence: moderate
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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 →