27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We used an untargeted mass spectrometric approach, tandem mass tag proteomics, for the identification of proteomic signatures in genetic frontotemporal dementia (FTD). 5 key findings →
Participants: 238 Evidence: low
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This study suggests that larger head circumference is associated with less cognitive impairment in the face of cerebral atrophy. 3 key findings →
Design: cross-sectional Participants: 270 Evidence: low
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A new interview schedule for the diagnosis and measurement of dementia in the elderly is described. 3 key findings →
Evidence: low
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The global prevalence of dementia is estimated to be as high as 24 million, and is predicted to double every 20 years through to 2040, leading to a costly burden of disease. 5 key findings →
Evidence: low
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Given considerable variation in diagnostic and therapeutic practice, there is a need for national guidance on the use of neuroimaging, fluid biomarkers, cognitive testing, follow-up and diagnostic terminology in mild cognitive impairment (MCI). 1 key finding →
Evidence: low
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Over the past decade it has become evident that a substantial minority of patients with primary dementing diseases, particularly those presenting in the presenium, have dementia of frontal lobe type (DFT) due to non-Alzheimer's pathology. 1 key finding →
Design: longitudinal study Participants: 52 Evidence: moderate
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Neurodegenerative disorders of ageing (NDAs) such as Alzheimer disease, Parkinson disease, frontotemporal dementia, Huntington disease and amyotrophic lateral sclerosis represent a major socio-economic challenge in view of their high prevalence yet poor treatment. 5 key findings →
Evidence: low
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Serine protease inhibitors (serpins), the acute phase reactants and regulators of the proteolytic processing of proteins, have been recognized as potential contributors to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Participants: 258 Evidence: low
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We developed and validated the Mini-Addenbrooke's Cognitive Examination (M-ACE) in dementia patients. 4 key findings →
Participants: 25 Evidence: low
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Amyotrophic lateral sclerosis overlapping with frontotemporal dementia (ALS/FTD) is a fatal and currently untreatable disease characterized by rapid cognitive decline and paralysis. 4 key findings →
Evidence: low
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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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Patients with mild cognitive impairment (MCI) were assessed, and a metabolic profile associated with conversion to AD at 18-month follow-up was sought.
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Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
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To examine the possibility that senile dementia may be associated with a loss of noradrenergic neurons that innervate the cerebral cortex, we used a Quantimet 720 image analyzer to estimate the number of neurons in the nucleus locus ceruleus in elderly patients with the clinical diagnosis of senile dementia. 1 key finding →
Evidence: low
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See Mercado and Hetz (doi:10.1093/brain/awx107) for a scientific commentary on this article. 1 key finding →
Evidence: low
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The identification of mutations in the Tau gene in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has made it possible to express human tau protein with pathogenic mutations in transgenic animals. 5 key findings →
Evidence: low
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Increasing numbers of people are developing type 2 diabetes mellitus, but interventions to prevent and treat the classic microvascular and macrovascular complications have improved, so that people are living longer with the condition. 2 key findings →
Evidence: high
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Alpha-synuclein forms the major component of Lewy bodies and Lewy neurites, the defining neuropathological characteristics of Parkinson's disease and dementia with Lewy bodies. 1 key finding →
Evidence: low
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Alzheimer's disease (AD) is increasingly recognized as a disconnection syndrome, which leads to cognitive impairment due to the disruption of functional activity across large networks or systems of interconnected brain regions. 4 key findings →
Participants: 18 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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The hippocampus is the brain structure of highest and earliest structural alteration in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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Single-cell RNA sequencing data generated with SmartSeq2 (≈8000 genes/cell) in 16 588 single cells isolated during atherosclerosis progression in Ldlr -/- Apob 100/100 mice with human-like plasma lipoproteins and from humans with asymptomatic and symptomatic carotid plaques was clustered into multiple subtypes. 4 key findings →
Evidence: low
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Microglial activation participates in white matter injury after cerebral hypoperfusion. 4 key findings →
Participants: 80 Evidence: low
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We report five patients with a stereotyped clinical syndrome characterized by fluent dysphasia with severe anomia, reduced vocabulary and prominent impairment of single-word comprehension, progressing to a stage of virtually complete dissolution of the semantic components of language.
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APP gene dosage is strongly associated with Alzheimer's disease (AD) pathogenesis. 3 key findings →
Evidence: preliminary
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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 27,780 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 →