28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Gut microbial metabolites serve as functional mediators of gut–brain communication, linking microbial alterations to neurodegenerative pathology. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
18F-MK-6240 (18F-labeled 6-(fluoro)-3-(1H-pyrrolo[2,3-c]pyridin-1-yl)isoquinolin-5-amine) is a highly selective, subnanomolar-affinity PET tracer for imaging neurofibrillary tangles (NFTs). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found strong evidence that plasma p-tau 181 is elevated in ALS and may be a novel marker specific to LMN dysfunction. 4 key findings →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source
Breakdown of the neurovascular unit is associated with blood-brain barrier (BBB) leakiness contributing to cognitive decline and disease pathology in the early stages of Alzheimer's disease (AD). 3 key findings →
Participants: 121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer's disease (AD) neuropathologic change and clinical stage. 1 key finding →
Participants: 388 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers such as tau phosphorylated at threonine 181 (phosphorylated-tau181) represent an accessible, cost-effective and scalable approach for the in vivo detection of Alzheimer's disease pathophysiology. 5 key findings →
Participants: 103 Evidence: low
Full summary, score breakdown and related studies → Original source
In the tea-consuming group, the MoCA scores ( P = 0.000), Hopkins Verbal Learning Test (HVLT) immediate recall ( P = 0.012) and delayed recall ( P = 0.013) were significantly higher while Trail Making Test-B ( P = 0.005) and Victoria Stroop test interference ( P = 0.000) were lower. 5 key findings →
Participants: 264 Evidence: low
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
The GM data are linked to the retrospective DPUK cohort dataset, including genotypic and longitudinal phenotypic data. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
However, there is growing recognition of the significant impact of motor dysfunction in individuals affected by AD. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Changes in the mitochondrial DNA copy number (mtDNAcn) and increased mitochondrial DNA mutation burden have both been associated with neurodegenerative diseases and cognitive decline. 5 key findings →
Participants: 1,361 Evidence: low
Full summary, score breakdown and related studies → Original source
Beta-amyloid deposition is a defining feature of Alzheimer's disease (AD). 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The analytic sample included 469 participants (mean age 71.2 ± 8.5 years, 53% female). 3 key findings →
Design: cohort Participants: 469 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
Previously derived polygenic risk scores (PRSs) for Alzheimer's disease (AD) perform inconsistently across diverse ancestries. 3 key findings →
Design: cohort Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The combined measure of CSF Abeta42 and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders. 4 key findings →
Participants: 84 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that inflammation in the CNS increases in normal aging and is intimately related to markers of neurodegeneration in the preclinical stages of AD and SNAP. sAPPβ and β-secretase activity are not useful diagnostic or staging markers in preclinical AD. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. 3 key findings →
Participants: 2,478 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is a progressive neurodegenerative disease most often associated with memory deficits and cognitive decline, although less common clinical presentations are increasingly recognized. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We detected large numbers of HLA-DR-positive reactive microglia (macrophages), along with Lewy bodies and free melanin, in the substantia nigra of all cases studied with Parkinson's disease (5) and parkinsonism with dementia (PD) (5). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CLBs detected by alpha-synuclein antibodies in patients with PD are a more sensitive and specific correlate of dementia than the presence of Alzheimer's pathology, which was present in a minority of the cases in this series. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Early reports of cognitive and behavioural deficits in motor neuron disease might have been overlooked initially, but the concept of a frontotemporal dementia-motor neuron disease continuum has emerged during the past decade. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The blood-brain barrier (BBB) is a continuous endothelial membrane within brain microvessels that has sealed cell-to-cell contacts and is sheathed by mural vascular cells and perivascular astrocyte end-feet. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postmortem MRI scans were obtained for the first 56 participants of the Nun Study who were scanned. 1 key finding →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 7,799 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →