30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Haploinsufficiency of progranulin (PGRN) causes frontotemporal dementia (FTD), a devastating neurodegenerative disease with no effective treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-based biomarker (BBM) profiles associated with genetic susceptibility to Alzheimer’s disease (AD) in general older populations remain poorly understood. 3 key findings →
Participants: 3,947 Evidence: low
Full summary, score breakdown and related studies → Original source
NOS1AP is an adaptor for neuronal nitric oxide synthase that engages several partner proteins and is implicated in Alzheimer’s disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based neurofilament light (NfL) is associated with all-cause mortality, but whether this reflects neuroaxonal injury or overlaps with cognitive and functional decline remains unclear. 3 key findings →
Participants: 559 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Interventions targeting lifestyle and health behaviors support cognition in older adults at risk of dementia. 5 key findings →
Participants: 1,260 Evidence: high
Full summary, score breakdown and related studies → Original source
NOS1AP is a genetically validated driver of tau pathology in Alzheimer’s disease (AD), yet the NOS1AP-tau interaction itself has remained pharmacologically untargeted. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Public interest in cannabinoid medicines has outpaced the clinical pharmacology needed to judge product, dose and route. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular cold-inducible RNA-binding protein (eCIRP) is a crucial neuroinflammatory mediator in ischemic stroke and alcohol-induced memory impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
SHED exosome treatment demonstrated genotype-specific efficacy, selectively reducing p181-tau levels and restoring the p181-tau/Aβ42 ratio in FAD lines while elevating the protective Aβ42/Aβ40 ratio across both FAD and SAD backgrounds. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a core driver of Alzheimer’s disease (AD) progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early neuronal hyperexcitability is a hallmark of Alzheimer’s disease (AD) and correlates with cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impaired peripheral clearance of amyloid-β (Aβ) contributes to Alzheimer's disease (AD) pathogenesis. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Chimpanzees share a number of age-related brain changes with humans, such as reductions in neurons and increases in neuropathology. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chronic Wasting Disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) that is confined to cervids (deer, moose, elk, and reindeer) but shares key properties with human neurodegenerative conditions such as Alzheimer’s, Parkinson’s, Huntington’s disease and frontal-temporal dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease primarily affecting motor neurons but also frequently involving cognitive impairment. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chitinase-3-like protein 1 (CHI3L1) is elevated in Alzheimers disease (AD), but its role in glial dysfunction and therapeutic tractability remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β (Aβ) plaques are a hallmark of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choroid plexus (CP) maintains brain homeostasis through cerebrospinal fluid production and formation of the blood-cerebrospinal fluid barrier, and its dysfunction has been linked with aging and neurological disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic variation in APOE , which encodes a lipid transporter apolipoprotein E (apoE), is the strongest risk factor for late-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the primary matched-feature comparison, reference areas under the receiver operating characteristic curve (AUCs) were 0.851 for ADNI tau90, 0.860 for ADNI tau180, and 0.933 for OASIS3 tau180. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 8,313 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →