Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. 4 key findings →
Participants: 1,716 Evidence: low
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. 4 key findings →
Participants: 1,716 Evidence: low
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We report duplication of the APP locus on chromosome 21 in five families with autosomal dominant early-onset Alzheimer disease (ADEOAD) and cerebral amyloid angiopathy (CAA). 3 key findings →
Evidence: low
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The data do not support an association between serum total cholesterol or high density lipoprotein in late life and subsequent risk of dementia or Alzheimer disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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APOE epsilon4 carrier status was associated with conversion to AD in older outpatients after controlling for known demographic and clinical risk factors, and APOE epsilon4 homozygosity was associated with increased risk of conversion to AD. 3 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
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Obesity at midlife is associated with an increased risk of dementia and AD later in life. 3 key findings →
Participants: 1,449 Evidence: low
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Raloxifene at a dose of 120 mg/day, but not 60 mg/day, resulted in reduced risk of cognitive impairment in postmenopausal women. 3 key findings →
Evidence: high
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It was possible to assign all patients to one of the PD stages. 2 key findings →
Participants: 88 Evidence: moderate
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Over an average follow-up of 4 y, dementia developed in 112 subjects, including 70 who received a diagnosis of AD. 3 key findings →
Design: cross-sectional Participants: 816 Evidence: moderate
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During follow-up, 13 healthy patients converted to MCI or Alzheimer disease (AD), whereas 39 MCI subjects converted to AD. 5 key findings →
Participants: 72 Evidence: low
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These results indicate that markers of systemic inflammation confer a statistically significant additional risk for cardiovascular death among patients with RA, even after controlling for traditional cardiovascular risk factors and comorbidities. 3 key findings →
Participants: 354 Evidence: moderate
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We have previously reported a large Danish pedigree with autosomal dominant frontotemporal dementia (FTD) linked to chromosome 3 (FTD3). 2 key findings →
Evidence: low
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A total of 533 patients with AD at early stages (mean Folstein Mini-Mental State Examination [MMSE] 21/30 at entry) were recruited and followed semiannually for up to 13.1 years (mean 3) in five University-based AD centers in the United States and European Union. 4 key findings →
Participants: 533 Evidence: moderate
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Cognitive functions and self-reported drinking habits were assessed at 2-year intervals over an average of 7 years of follow-up. 4 key findings →
Design: longitudinal study Evidence: moderate
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Because cardiovascular (CV) risk factors have been associated with declines in cognitive functions and late life dementia, CV risk factors should also be associated with brain atrophy. 4 key findings →
Participants: 1,812 Evidence: moderate
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Thirty-two percent of residents had DNR directives, whereas less than 2% had DNH directives. 5 key findings →
Design: cohort study Participants: 1,962,742 Evidence: moderate
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Alzheimer's disease (AD) and antecedent factors associated with AD were explored using amyloid imaging and unbiased measures of longitudinal atrophy in combination with reanalysis of previous metabolic and functional studies.
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Specific alleles of the DISC1 and TRAX genes on 1q42 appear to contribute to genetic risk for schizophrenia through disruptive effects on the structure and function of the prefrontal cortex, medial temporal lobe, and other brain regions. 2 key findings →
Design: cohort study Evidence: moderate
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The diagnosis of Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI) is limited because it is based on non-specific behavioral and neuroimaging findings. 3 key findings →
Design: longitudinal study Evidence: moderate
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Neither quetiapine nor rivastigmine are effective in the treatment of agitation in people with dementia in institutional care. 4 key findings →
Participants: 93 Evidence: high
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Donepezil was well tolerated and most adverse events were mild. 5 key findings →
Participants: 22 Evidence: high
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Cholesterol-induced production of amyloid beta (Abeta) as a putative neurotoxin in Alzheimer's disease (AD), along with epidemiological evidence, suggests that statin drugs may provide benefit in treatment of the disorder. 5 key findings →
Participants: 98 Evidence: high
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Alzheimer disease was responsible for 4.9% of the deaths in this elderly cohort. 1 key finding →
Participants: 1,670 Evidence: moderate
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We prospectively evaluated the diagnostic accuracy of cerebrospinal fluid (CSF)-beta-amyloid1-42 (Abeta42), -total-tau (tau) and -phosphorylated-tau181 (p-tau181) as measured by sandwich ELISAs in the clinical routine of a community state hospital to discriminate between patients with Alzheimer's disease (AD), healthy controls (HC), non-AD-dementias, a group composed of various psychiatric disorders (non-AD-dementias, mental diseases) and an age-matched random sample (RS) (total N=219). 4 key findings →
Participants: 219 Evidence: low
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CERAD total scores were obtained by summing scores from the individual CERAD subtests (excluding the Mini-Mental State Examination [MMSE]) into a total composite (maximum score = 100). 4 key findings →
Participants: 424 Evidence: low
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According to all previous literature, they are not associated with mortality. 4 key findings →
Participants: 456 Evidence: moderate
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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 →