28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF A beta(1-42) was the most sensitive biomarker for AD in the autopsy cohort of CSF samples: receiver operating characteristic area under the curve of 0.913 and sensitivity for AD detection of 96.4%. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study proposes a model that relates disease stages to Alzheimer's disease biomarkers.
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amnestic mild cognitive impairment (aMCI) is considered a prodromal stage of Alzheimer's disease (AD). 2 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A highly robust assay for repeatedly measuring Abeta forms in plasma such as INNO-BIA plasma Abeta forms might be a useful tool in a future risk assessment of AD. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Reduction in CSF Abeta(42), likely reflecting Abeta aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
In a population-based sample, increasing gliosis precedes development of Alzheimer lesions. 3 key findings →
Evidence: moderate
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The use of frozen rather than fresh samples renders higher diagnostic accuracy within a multicentre context. 2 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
The clinical diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD) is difficult, and reliable markers are highly desired. 2 key findings →
Participants: 71 Evidence: low
Full summary, score breakdown and related studies → Original source
The human GFAP splice variants GFAPDelta164 and GFAPDeltaexon6 both result in a GFAP protein isoform with a unique out-of-frame carboxy-terminus that can be detected by the GFAP+1 antibody. 3 key findings →
Evidence: low
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The excitotoxin quinolinic acid (QUIN) is synthesized through the kynurenine pathway (KP) by activated monocyte lineage cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) refers to the specific deposition of amyloid fibrils in the leptomeningeal and cerebral blood vessel walls, often causing secondary vascular degenerative changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of astrocytes has been known to be associated with amyloid-beta (Abeta) deposit and production of pro-inflammatory cytokines and chemokines that lead to neuronal cell death in the pathogenesis of Alzheimer disease (AD). 5 key findings →
Evidence: low
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Advances in our understanding of tau-mediated neurodegeneration in Alzheimer's disease (AD) are moving this disease pathway to center stage for the development of biomarkers and disease modifying drug discovery efforts. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurovascular unit (NVU) comprises cerebral blood vessels and surrounding astrocytes, neurons, perivascular microglia and pericytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress is involved in many neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in presenilin (PS) and amyloid precursor protein (APP) genes are a predominant cause for early-onset familial Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by amyloid plaques and neurofibrillary tangles associated with chronic inflammation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disturbed homocysteine metabolism is a risk factor for Alzheimer's disease (AD) and may contribute to the disease pathophysiology by increasing both amyloid-beta (Abeta) production and phosphorylated tau (P-tau) accumulation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with senile beta-amyloid (Abeta) plaques and cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic cerebral ischemia may accelerate clinicopathological changes in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common type of dementia, comprising 60-80% of all reported cases, and currently affects 5.2 million Americans. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The association of increased CSF-NFL levels with increasing severity of WMLs in non-demented subjects suggests that NFL is a marker for axonal damage in response to small vessel disease in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) and protein S-100B are established indicators of astrogliosis in neuropathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In mammalian central nervous system, neurogenesis occurs in the hippocampus and the subventricular zone (SVZ). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →