27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare form of vasculitis associated with amyloid-β (Aβ) deposition in vessel walls, has been proposed as a spontaneous human model of the amyloid-related imaging abnormalities (ARIA) occurring after anti-Aβ immunotherapy for the treatment of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-related imaging abnormalities (ARIA), thought to reflect immune responses to vascular amyloid, have been detected in several amyloid-modifying therapy trials for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In addition to a prominent role in glycemic control, glucagon-like peptide 1 (GLP-1) receptor agonists exhibit neuroprotective properties. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The NOD-like receptor (NLR) family, pyrin domain-containing protein 3 (NLRP3) inflammasome is a component of the inflammatory process, and its aberrant activation is pathogenic in inherited disorders such as cryopyrin-associated periodic syndrome (CAPS) and complex diseases such as multiple sclerosis, type 2 diabetes, Alzheimer's disease and atherosclerosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Misfolded protein aggregates represent a continuum with overlapping features in neurodegenerative diseases, but differences in protein components and affected brain regions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological assembly of Aβ, tau, and α-synuclein is at the heart of Alzheimer's and Parkinson's diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammation is a pathological hallmark of Alzheimer's disease, and innate immune cells have been shown to contribute to disease pathogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
SMC ε4+ showed greater amyloid deposition than SMC ε4-, but no hypometabolism or medial temporal lobe (MTL) atrophy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Until recently, estimation of β-amyloid plaque density as a key element for identifying Alzheimer's disease (AD) pathology as the cause of cognitive impairment was only possible at autopsy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The volumes of the presubiculum and subiculum presented the most remarkable reduction in the patient's groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We detected immunoreactivity for all proteins along the optic pathway. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All but one patient showed one or more neuropsychiatric symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with prior AD diagnosis used substantially more medical services every year until their VD/PD diagnosis, resulting in incremental annual medical costs of approximately $9,500-$14,000. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropsychological tests, CSF markers, and hippocampal volume predicted conversion from MCI to AD and general dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results confirm the key role of CSF biomarkers in predicting patient conversion from MCI to dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is characterized neuropathologically by synaptic disruption, neuronal loss, and deposition of amyloid β (Aβ) protein in brain structures that are critical for memory and cognition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Exposure to stress is one of the best-known negative regulators of adult neurogenesis (AN). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that DTI data provide better prediction accuracy than GM volume in predementia AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hyperphosphorylation and dysregulation of exon 10 splicing of Tau are pivotally involved in pathogenesis of Alzheimer disease (AD) and/or other tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune-modulatory receptor involved in phagocytosis and inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation occurs in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nursing homes generally met three quarters of the pre-defined criteria for advance care planning policy. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
These data reveal a link between reduced glucocerebrosidase and the development of α-synucleinopathy and pathophysiological abnormalities in mice, and support the development of GCase therapeutics to reduce α-synucleinopathy in PD and related disorders. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overexpression of apoE isoforms induces differential effects in the apoE4-TR background: apoE4 decreases apoE lipidation and enhances Aβ accumulation, whereas apoE2 has the opposite effects. 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →