In chronic liver failure, manganese accumulation is responsible for the pallidal MRI T1 hyperintensity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In chronic liver failure, manganese accumulation is responsible for the pallidal MRI T1 hyperintensity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We compare patterns of gray matter loss on MRI in subjects presenting as corticobasal syndrome (CBS) with Alzheimer disease pathology (CBS-AD) to those presenting as CBS with corticobasal degeneration pathology (CBS-CBD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Accurate assessment of cognitive impairment requires comparison of cognitive performance in individuals to performance in a comparable healthy normative population. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Machine learning has become ubiquitous and a key technology on mining electronic health records (EHRs) for facilitating clinical research and practice. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma biomarkers such as phospho-tau species are increasingly used in clinical practice for the diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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BackgroundAlzheimer's disease (AD) and related dementias are leading causes of death worldwide. 4 key findings →
Participants: 6,909 Evidence: moderate
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Amyloid PET enables improved detection of amyloid-β plaques within the brain. 5 key findings →
Evidence: low
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Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2). 5 key findings →
Design: longitudinal study Evidence: moderate
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Lewy body dementia (LBD), which includes dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), is characterized by cognitive decline, sleep disturbances, motor dysfunction, and other debilitating clinical symptoms. 2 key findings →
Evidence: low
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We identified a significant genome-wide association with p-S65-Ub for rs429358 (apolipoprotein E ε4 [APOE4]) and a suggestive association for rs6480922 (ZMIZ1). 5 key findings →
Evidence: low
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DLB with rapid cognitive decline showed greater CA1 αSYN oligomer burden (p = 0.029) and tau burden (p = 0.029) than DLB with slow decline. 5 key findings →
Evidence: low
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This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
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For many years, blood-based biomarkers for Alzheimer's disease seemed unattainable, but recent results have shown that they could become a reality. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Overexpression of Alzheimer amyloid precursor protein (APP) produces dramatically different phenotypes in transgenic mice depending on the genetic background. 1 key finding →
Evidence: low
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This article presents a wavelet coherence investigation of electroencephalograph (EEG) readings acquired from patients with Alzheimer disease (AD) and healthy controls. 4 key findings →
Evidence: low
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Cerebral white matter hyperintensities on brain MRI (leukoaraiosis) are associated with increased risk of stroke and dementia. 5 key findings →
Evidence: low
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Features for rule-based systems, including significant words and patterns related to SBI, were generated using pointwise mutual information. 3 key findings →
Evidence: low
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The field of aging and dementia research is advancing rapidly toward the stage of earlier identification of clinical symptoms. 5 key findings →
Evidence: low
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Global PSP prevalence ranges between 5-6.4 per 100,000, influenced by diagnostic criteria and healthcare infrastructure. 5 key findings →
Evidence: low
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Typical normative models appear appropriate for remote self‐administered measures and are sensitive to cognitive impairment. 3 key findings →
Participants: 167 Evidence: low
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Alzheimer disease (AD) is the leading cause of dementia, with an estimated 6.9 million Americans aged 65 and older living with Alzheimer dementia today, with this number projected to grow to 13.8 million by 2060. 5 key findings →
Evidence: low
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Dementia with Lewy bodies (DLB), a progressive neurodegenerative disease with heterogeneous clinical presentations, greatly impacts patients, caregivers, and society. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Area under the receiver operating characteristic curves differentiating PSP and controls were improved by PC1 subtraction in the frontal white matter (0.54 to 0.67; P = 0.002) and subcortical (0.69 to 0.87; P < 0.001) regions. 4 key findings →
Participants: 141 Evidence: moderate
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Accurate estimation of Alzheimer's disease (AD) severity from structural magnetic resonance imaging (MRI) remains difficult, as disease-associated anatomical alterations are often subtle and publicly available datasets are typically too small to support robust deep learning model training. 1 key finding →
Participants: 214 Evidence: moderate
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Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. 1 key finding →
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →