27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
There is accumulating evidence that synaptic loss precedes neuronal loss and correlates best with impaired memory formation in Alzheimer's disease (AD). 4 key findings →
Participants: 52 Evidence: low
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Mid-life obesity is an established risk factor for Alzheimer's disease (AD) dementia, whereas late-life obesity has been proposed as a protective state. 4 key findings →
Participants: 162 Evidence: low
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Alzheimer's disease (AD) is the most common cause of progressive dementia in the elderly. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Since the discovery of CSF1R gene mutations in families with hereditary diffuse leukoencephalopathy with spheroids in 2012, more than 70 different mutations have been identified around the world. 4 key findings →
Evidence: low
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Between 2000 and 2015, deaths resulting from stroke, heart disease, and prostate cancer decreased, whereas deaths from AD increased 123%.
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Cardiovascular risk factors, deregulated blood glucose, uric acid metabolism, and inflammation were identified as risk markers for faster disease progression. 2 key findings →
Participants: 135 Evidence: moderate
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CSF biomarkers and amyloid positron emission tomography reflect different aspects of Alzheimer's disease brain pathology, and therefore, less-than-perfect correspondence is expected. 1 key finding →
Participants: 200 Evidence: low
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These findings provide additional insight into gut microbial involvement in AD and add to the growing understanding of the gut-brain axis. 2 key findings →
Participants: 410 Evidence: low
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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
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Magnetic resonance-guided focused ultrasound in combination with intravenously injected microbubbles has been shown to transiently open the blood-brain barrier, and reduce beta-amyloid and tau pathology in animal models of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to explore the risk of dementia in a middle- and older-aged population with severe or profound hearing impairments. 3 key findings →
Evidence: moderate
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Further investigations are needed to elaborate how the concept of a key contact person could be integrated with existing case management approaches and how the independence and autonomy of people with dementia can be strengthened when formal care needs to be accessed and used. 1 key finding →
Participants: 261 Evidence: low
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Accurate and early diagnosis of Alzheimer's disease (AD) plays important role for patient care and development of future treatment. 1 key finding →
Participants: 397 Evidence: low
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Among the hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by the A/T/N classification. 3 key findings →
Participants: 70 Evidence: low
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Familial Alzheimer's disease (FAD) is characterized by a positive family history of dementia and typically occurs at an early age with an autosomal dominant pattern of inheritance. 2 key findings →
Participants: 15 Evidence: low
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The authors plan to reevaluate ACP statistics in the same office following a future intervention. 2 key findings →
Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
In patients treated up to 36 months, amyloid plaque levels continued to decrease in a dose- and time-dependent manner, with levels in the 10 mg/kg fixed-dose group reaching and remaining below a quantitative cut-point discriminating a positive/negative scan. 1 Reduced amyloid plaque levels were also observed in patients switched from placebo to aducanumab during the LTE. 5 key findings →
Design: clinical trial Evidence: high
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GWAS found the associations of two single nucleotide polymorphisms (rs7943454 and rs640476) with plasma NFL at suggestive levels. 5 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
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In the initial kindred of ten affected Italian individuals (mean age of disease onset 59·8 years [SD 8·7]), we detected significant linkage of Parkinson's disease to chromosome 14 and nominated LRP10 as the disease-causing gene. 2 key findings →
Evidence: low
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Among 104 537 individuals, the absolute 10-year risk of Alzheimer disease in 3017 women and men who were carriers of the APOE ɛ44 genotype was, respectively, 7% and 6% at age 60-69 years, 16% and 12% at age 70-79 years, and 24% and 19% at age 80 years and older. 1 key finding →
Participants: 537 Evidence: low
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Falls remain common in older people, with higher prevalence and morbidity in those who are cognitively impaired. 1 key finding →
Evidence: low
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We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). 3 key findings →
Evidence: low
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Older people with cognitive impairment have a higher risk of a variety of negative outcomes in hospital. 4 key findings →
Evidence: low
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Intronic GGGGCC repeat expansions in C9orf72 are the most common known cause of frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), which are characterised by degeneration of cortical and motor neurons, respectively. 2 key findings →
Evidence: low
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There is no disease-modifying treatment currently available for AD, one of the more impacting neurodegenerative diseases affecting more than 47.5 million people worldwide. 1 key finding →
Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 →