These data suggest that beta-HCH is associated with a diagnosis of PD. 4 key findings →
Design: case-control study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
These data suggest that beta-HCH is associated with a diagnosis of PD. 4 key findings →
Design: case-control study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid tau and CSF-Abeta42 have so far been studied in research settings, under conditions providing data on the optimal performance. 1 key finding →
Participants: 105 Evidence: low
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This risk score could be used to identify persons at risk of LOAD, but can also be used to adjust for confounders in epidemiologic studies. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The APOE epsilon4 allele appears to be associated with a higher prevalence of dementia in PD. 1 key finding →
Design: case-control study Evidence: moderate
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Family history of dementia was associated with an increased risk of dementia and AD in this very old population, but only among APOE epsilon4 carriers. 5 key findings →
Design: cohort study Participants: 907 Evidence: moderate
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Ninety-nine new cases of dementia (including 71 of Alzheimer disease) occurred during the follow-up. 4 key findings →
Evidence: low
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An international group of clinical and basic scientists participated in the Frontotemporal Dementia and Pick's Disease Criteria Conference at the National Institutes of Health in Bethesda, Md, on July 7, 2000, to reassess clinical and neuropathological criteria for the diagnosis of frontotemporal dementia (FTD). 4 key findings →
Evidence: low
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Patients with MCI had a predominant memory impairment with relative sparing of other cognitive domains and were intermediate between clinically normal individuals and patients with AD on cognitive and functional ratings. 3 key findings →
Participants: 769 Evidence: low
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The INNOTEST and INNO-BIA CSF platforms perform equally well in identifying individuals with underlying amyloid plaque pathology. 2 key findings →
Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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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In contrast to observations in individuals not treated with CART, we found no relationship between CSF markers and neurological status in this CART-using cohort with advanced HIV/AIDS. 2 key findings →
Design: cohort study Participants: 106 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Semantic dementia is distinguishable from other presentations of frontotemporal dementia and Alzheimer disease, not only by fluent speech and impaired comprehension without loss of episodic memory, syntax, and phonology but also by empty, garrulous speech with thematic perseverations, semantic paraphasias, and poor category fluency. 2 key findings →
Design: cohort study Participants: 48 Evidence: moderate
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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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At autopsy the striatal dopaminergic transporter is reduced. 4 key findings →
Design: cohort study Evidence: moderate
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High HDL-C levels in elderly individuals may be associated with a decreased risk of AD. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
CST3 is a susceptibility gene for late-onset AD, especially in patients aged 75 years and older. 2 key findings →
Design: case-control study Participants: 260 Evidence: moderate
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These data suggest significant treatment benefits of donepezil in early-stage Alzheimer disease, supporting the initiation of therapy early in the disease course to improve daily cognitive functioning. 3 key findings →
Participants: 96 Evidence: high
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The "preclinical phase" of detectable lowering of cognitive functioning precedes the appearance of pAD by many years. 2 key findings →
Participants: 1,076 Evidence: low
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Mean plasma Abeta40 levels were higher in the AD group than in controls (P = .005), but there was substantial overlap; Abeta42 levels were similar between the groups. 4 key findings →
Participants: 78 Evidence: low
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Cross-sectional and longitudinal observation. 2 key findings →
Design: cross-sectional Evidence: moderate
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Cerebrovascular compromise of the cholinergic pathways may be a factor that contributes more selectively than does total white matter lesion burden to response to cholinergic therapy in Alzheimer disease, particularly on frontal/executive tasks. 3 key findings →
Design: cohort study Evidence: moderate
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Demographic and clinical factors impact PD survival. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Patients with progressive dementia invariably evolve to a stage where they can no longer be tested by standard neuropsychological tests. 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
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Alzheimer disease (AD) is the most common form of dementia worldwide. 4 key findings →
Design: cross-sectional Participants: 24 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neuronal degeneration and dopamine loss in the preclinical phase of Parkinson disease may produce subtle complaints before clinically recognizable symptoms emerge. 4 key findings →
Design: cohort study Participants: 6,038 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →