Plasma levels of glial fibrillary acidic protein (GFAP) and neurofilament light (NEFL) are key dementia biomarkers. 3 key findings →
Participants: 50,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma levels of glial fibrillary acidic protein (GFAP) and neurofilament light (NEFL) are key dementia biomarkers. 3 key findings →
Participants: 50,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Studies suggest that dysfunction of brain-derived neurotrophic factor (BDNF) is a possible contributor to the pathology and symptoms of Alzheimer's disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Genome-wide association studies (GWAS) have identified polymorphism in the Apolipoprotein E gene (APOE) to be the most prominent risk factor for Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although sleep, physical activity and sedentary behavior have been found to be associated with dementia risk, findings are inconsistent and their joint relationship remains unclear. 4 key findings →
Participants: 431,924 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Psychotic symptoms occur in ~40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional deficits. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma neurofilament light (NfL) protein is a promising non-invasive biomarker for detecting neuronal damage in Alzheimer's disease (AD). 5 key findings →
Participants: 860 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Physical and cognitive exercise may prevent or delay dementia in later life but the neural mechanisms underlying these therapeutic benefits are largely unknown. 3 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Late-life depression (LLD) has been linked to increased likelihood of dementia, although mechanisms responsible for this association remain largely unknown. 3 key findings →
Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Ferritin, an iron storage and regulation protein, has been associated with Alzheimer's disease (AD); however, it has not been investigated in preclinical AD, detected by neocortical amyloid-β load (NAL), before cognitive impairment. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
People's differences in cognitive functions are partly heritable and are associated with important life outcomes. 5 key findings →
Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Arousal affects cognition, emotion, and behavior and has been implicated in the etiology of psychiatric disorders. 5 key findings →
Participants: 1,877 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The innate immune system plays an integral role in the progression of many neurodegenerative diseases. 4 key findings →
Participants: 148 Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) dependent lifetime risks (LTRs) for Alzheimer Disease (AD) are currently not accurately known and odds ratios alone are insufficient to assess these risks. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Short-term memory dysfunction is a key early feature of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study was designed to evaluate whether subjects with amyloid beta (Aβ) pathology, detected using florbetapir positron emission tomorgraphy (PET), demonstrated greater cognitive decline than subjects without Aβ pathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Deposition of amyloid-β (Aβ) in the cerebral cortex is thought to be a pivotal event in Alzheimer's disease (AD) pathogenesis with a significant genetic contribution. 3 key findings →
Participants: 555 Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytes can adopt multiple molecular phenotypes in the brain of Alzheimer's disease (AD) patients. 4 key findings →
Participants: 121 Evidence: low
Full summary, score breakdown and related studies → Original source
The associations of synaptic loss with amyloid-β (Aβ) and tau pathology measured by positron emission tomography (PET) and plasma analysis in Alzheimer's disease (AD) patients are unknown. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid (Aβ) pathology is the earliest detectable pathophysiological event along the Alzheimer's continuum, which can be measured both in the cerebrospinal fluid (CSF) and by Positron Emission Tomography (PET). 2 key findings →
Participants: 320 Evidence: low
Full summary, score breakdown and related studies → Original source
With the advent of technologies that allow simultaneous genotyping of thousands of single-nucleotide polymorphisms (SNPs) across the genome, the genetic contributions to complex diseases can be explored at an unprecedented detail. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We previously developed a novel machine-learning-based brain age model that was sensitive to amyloid. 3 key findings →
Participants: 757 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOEε4 is the most well-established genetic risk factor for sporadic Alzheimer's disease and is associated with cerebral amyloid-β. 4 key findings →
Participants: 211 Evidence: low
Full summary, score breakdown and related studies → Original source
A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mechanisms underlying the protective effect of apolipoprotein E (APOE) ε2 against Alzheimer disease (AD) are not well understood. 4 key findings →
Participants: 982 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 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 →