27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
FDA-approved anti-Aβ mabs have a role in slowing disease progression in patients with AD, at the cost of an increased probability of side effects. 3 key findings →
Design: systematic review Participants: 4,471 Evidence: high
Full summary, score breakdown and related studies → Original source
These results provide new insight into the genetic basis of habitual PA, and the genetic links connecting PA with other traits and diseases. 5 key findings →
Design: meta-analysis Participants: 8,556 Evidence: high
Full summary, score breakdown and related studies → Original source
A rare TREM2 missense mutation (rs75932628-T) was reported to confer a significant Alzheimer's disease (AD) risk. 4 key findings →
Design: meta-analysis Participants: 89,157 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The purpose of this systematic review and meta-analysis was to evaluate the performance of cerebrospinal fluid (CSF) beta amyloid 42 (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau) as potential diagnostic biomarkers for idiopathic normal-pressure hydrocephalus (iNPH) and to assess their utility indistinguishing patients with iNPH from those with Alzheimer disease (AD) and healthy normal controls. 4 key findings →
Design: systematic review Participants: 413 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Oral benfotiamine is safe and potentially efficacious in improving cognitive outcomes among persons with MCI and mild AD. 5 key findings →
Design: randomized controlled trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cognitive performance in mild AD improved following tACS, with increased FC within cortical networks and between the hippocampus and specific cortical regions. 2 key findings →
Design: randomized controlled trial Participants: 23 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The forms of tau in CSF and plasma are distinct, but in each specimen type, the levels of certain fragments are increased in AD. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH), is an advanced stage of metabolic fatty liver disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
With the publication in 2015 of the consensus statement by the perfusion study group of the International Society for Magnetic Resonance in Medicine (ISMRM) and the EU-COST action 'ASL in dementia' on the implementation of arterial spin labelling MRI (ASL) in a clinical setting, the development of ASL can be considered to have become mature and ready for clinical prime-time. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High-intensity interval training (HIIT) alleviates cognitive dysfunction in STZ-induced AD-like rat models and provides neuroprotection against neurodegeneration, neuronal damage, and neuronal loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We revealed GLP-1's capacity to regulate astrocytic glycolysis, providing mechanistic insight into one of its neuroprotective roles in AD and support for the feasibility of energy regulation treatments for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuronal intranuclear inclusion disease (NIID) is a slowly progressing neurodegenerative disease characterized by eosinophilic intranuclear inclusions in the nervous system and multiple visceral organs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is closely linked to the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical studies have shown that epileptic seizures worsen Alzheimer's disease (AD) pathology and related cognitive deficits; however, the underlying mechanism is unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The role of mitochondrial dysfunction has been well-documented in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Iron has a role in brain injury after IVH. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent research on Alzheimer's disease (AD) has shown that cognitive and memory decline in this disease is accompanied by disrupted changes in the coordination of large-scale brain functional networks. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →
Participants: 58,876 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular risk factors were associated with CSVD burden and progression, and WMH and PVS progression were further associated with cortical atrophy and cognitive decline, underscoring the interconnected contributions of vascular risk, CSVD, and neurodegeneration to cognitive aging and dementia risk. 5 key findings →
Design: cross-sectional Participants: 289 Evidence: moderate
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 27,380 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 →