Dementia is common in Parkinson's disease (PD) but measures that track cognitive change in PD are lacking. 4 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Dementia is common in Parkinson's disease (PD) but measures that track cognitive change in PD are lacking. 4 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) can present with distinct clinical variants. 4 key findings →
Participants: 93 Evidence: low
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Cerebral microbleeds (CMBs), also referred to as microhemorrhages, appear on magnetic resonance (MR) images as hypointense foci notably at T2*-weighted or susceptibility-weighted (SW) imaging. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found a 2- to 3-fold geographical variation in dementia odds in Sweden, after twin random effects-likely to capture genetic and shared environmental variance-were removed. 5 key findings →
Participants: 27,680 Evidence: moderate
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This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease. 1 key finding →
Design: cross-sectional Evidence: low
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A total of 322 participants with p-tau217, GFAP, and NfL analyses were stratified into the EOAD or FTD group based on their diagnosis. 5 key findings →
Design: cohort study Participants: 245 Evidence: moderate
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We included 6879 persons (mean 56.1 years, standard deviation 6.2). 5 key findings →
Design: cohort study Participants: 6,879 Evidence: moderate
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When an individual with MCI-LB endorsed more clinical features, they typically experienced a faster cognitive decline (ACE-R Score Difference β = -1.1 [-1.7 to -0.5]), specifically when experiencing visual hallucinations (β = -2.1 [-3.5 to -0.8]) or cognitive fluctuations (β = -3.4 [-4.8 to -2.1]).Individuals with MCI-LB typically acquired more clinical features with the passage of time (25.5% [20.0-32.0%] one-year probability), limiting the prognostic utility of baseline-only features. 3 key findings →
Design: cohort study Participants: 74 Evidence: moderate
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Amyloid burden impacts cognitive decline in the pre-dementia stages of Alzheimer's disease (AD), but there remains significant variability in cognitive trajectories that may be explainable by markers of synaptic function and neurodegeneration. 2 key findings →
Design: longitudinal study Evidence: moderate
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The extent to which Alzheimer neuropathology, particularly the accumulation of misfolded beta-amyloid, contributes to cognitive decline and dementia in Parkinson's disease (PD) is unresolved. 1 key finding →
Design: cross-sectional Participants: 23 Evidence: low
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Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers. 4 key findings →
Participants: 319 Evidence: moderate
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Higher levels of neuroinflammation, neurodegeneration, and synaptic dysfunction in older adults were attenuated in KL-VS HET . 4 key findings →
Participants: 122 Evidence: moderate
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Diagnosing Alzheimer's disease (AD) in adults with Down syndrome (DS), a population with a high genetically determined risk of AD, remains challenging. 1 key finding →
Participants: 2,329 Evidence: low
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Mechanisms underlying phenotypic heterogeneity in young onset Alzheimer disease (YOAD) are poorly understood. 1 key finding →
Participants: 37 Evidence: low
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The authors estimated the effects of each of the three commonly used drugs for Alzheimer disease (donepezil, galantamine, and rivastigmine) in terms of predefined clinical outcomes and trial completion rates, by dosing level, and described differences among them. 4 key findings →
Evidence: low
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Imaging has played a variety of roles in the study of Alzheimer disease (AD) over the past four decades. 5 key findings →
Evidence: low
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Frontotemporal dementia (FTD) is the second most common young-onset dementia and is clinically characterised by progressive behavioural change, executive dysfunction and language difficulties. 1 key finding →
Evidence: low
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These findings suggest that the loss of perivascular AQP4 localization may contribute to the development of AD pathology in human populations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We performed hypothesis-free linkage analysis and exome sequencing in a family with two siblings who had neuronal ceroid lipofuscinosis (NCL). 3 key findings →
Evidence: low
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Deposits of abnormally phosphorylated tau protein are found in numerous neurodegenerative disorders; the 'tauopathies', which include Alzheimer's and Pick's diseases, but tau pathology is also found in the ageing brain. 2 key findings →
Evidence: moderate
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Baseline brain volume was lowest in AD but did not differ significantly between MCI, subjective complaints, and control groups (P > .38). 3 key findings →
Participants: 65 Evidence: low
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Alzheimer's disease is a genetically complex disorder; rare variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been shown to as much as triple an individual's risk of developing Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The hemizygous R47H variant of triggering receptor expressed on myeloid cells 2 ( TREM2 ), a microglia-specific gene in the brain, increases risk for late-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →