27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In Down syndrome, enhanced apoptosis (programmed cell death) may play a role in the pathogenesis of characteristic early mental retardation and precocious neurodegeneration of Alzheimer type. 2 key findings →
Evidence: low
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Apoptosis is the mechanism by which cells are programmed to die under a wide range of physiological and developmental stimuli. 3 key findings →
Evidence: low
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There is a limited choice of psychometric tests for Portuguese speaking people which have been evaluated in well defined groups. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular dementia (VaD) is the second commonest subtype of dementia after Alzheimer's disease (AD). 1 key finding →
Evidence: low
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Down syndrome (trisomy 21) is a genetic disease with developmental brain abnormalities resulting in early mental retardation and precocious, age dependent Alzheimer-type neurodegeneration. 3 key findings →
Evidence: low
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The measurement of CSF specimens from Netherlands Brain Bank showed that the levels of total tau and p-tau in CSF specimens of AD patients were significantly higher than those in CSF of patients with VD and non-dementia neurological disorders, and of age-matched non- 4 key findings →
Participants: 52 Evidence: low
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This review discusses the research published in the last five years on the behavioral, genetic, medical, and neuroscience aspects of Down syndrome. 2 key findings →
Evidence: low
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Complex interactions and interconnectivity between neurons are hallmarks of normal neuronal differentiation and development. 1 key finding →
Evidence: low
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Changes in the metabolic activity within the brain of patients suffering from Alzheimer's disease (AD) were investigated and compared with biochemical alterations in the hippocampus induced by fimbria/fornix transection in the rat. 5 key findings →
Evidence: low
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A neuropathological study of Alzheimer type I (Alz I) and Alzheimer type II (Alz II) as well as Opalski (Opl) cells was performed serially on brain tissue from nine autopsied Wilson's disease (WD) cases. 5 key findings →
Evidence: low
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Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome, as a phenotypic result of trisomy 21, is a complex condition with a set of over 30 phenotypic features, which manifest themselves with varying frequencies among affected individuals. 3 key findings →
Evidence: low
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Impaired glucose metabolism in adult Down Syndrome (DS) has been well-documented in vivo and information on the underlying biochemical defect i.e. aberrant glucose handling enzymes is already available. 2 key findings →
Evidence: low
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Symptoms of mania have been given inadequate attention as a source of agitated behavior in the dementia patient. 3 key findings →
Evidence: low
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The present study investigated the frequency and distribution of TUNEL-positive neurons in brains of dementia with Lewy bodies (DLB) in comparison with those in brains of Alzheimer's disease (AD), Down syndrome (DS) and non-demented elderly persons. 2 key findings →
Evidence: low
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Back to table of contents Previous article Next article Clinical & Research NewsFull AccessFew Alzheimer’s Patients Get State-of-Art CareJim RosackJim RosackSearch for more papers by this authorPublished Online:20 Apr 2001https://doi.org/10.1176/pn.36.8.0042Preliminary data suggest that a huge treatment gap exists in patients with Alzheimer’s disease, with as many as 65 percent of patients with the progressive and terminal disorder going undiagnosed and, therefore, untreated. 5 key findings →
Participants: 125 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Evidence: low
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 →