We present a new ARWMC scale applicable to both CT and MRI that has almost equal sensitivity, except for certain regions.
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27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We present a new ARWMC scale applicable to both CT and MRI that has almost equal sensitivity, except for certain regions.
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WMC severity and diabetes are independent predictors of cognitive decline in an initially nondisabled elderly population. 1 key finding →
Participants: 639 Evidence: low
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Geroscience, the new interdisciplinary field that aims to understand the relationship between aging and chronic age-related diseases (ARDs) and geriatric syndromes (GSs), is based on epidemiological evidence and experimental data that aging is the major risk factor for such pathologies and assumes that aging and ARDs/GSs share a common set of basic biological mechanisms. 2 key findings →
Evidence: low
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Females with sporadic bvFTD showed worse compulsive behavior (p = 0.026) and language impairments (p = 0.024) compared to females with genetic bvFTD (n = 152). 5 key findings →
Participants: 152 Evidence: low
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A total of 2540 records were screened. We included 10 studies. 5 key findings →
Design: systematic review Participants: 2,540 Evidence: high
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None of the participants were diabetics, smokers, or met criteria for obesity. 4 key findings →
Design: cross-sectional Evidence: moderate
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The purpose of this study was to investigate the prevalence of dementia in an Italian population using a door-to-door 2-phase design. 2 key findings →
Participants: 778 Evidence: low
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A careful clinical evaluation of sleep disorders should be performed routinely in the clinical setting of persons with cognitive decline. 1 key finding →
Evidence: moderate
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One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc). 2 key findings →
Evidence: low
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Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. 4 key findings →
Evidence: low
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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We found WMH and lacunes to be independently associated with general cognitive function in a sample of independently living elderly. 5 key findings →
Evidence: low
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Physical activity reduces the risk of cognitive impairment, mainly vascular dementia, in older people living independently. 1 key finding →
Participants: 90 Evidence: low
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Vascular dementia (VaD) incorporate different vascular mechanisms and changes in the brain, and have different causes and clinical manifestations. 5 key findings →
Evidence: low
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These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD. 3 key findings →
Evidence: low
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NfL holds potential as a blood-based biomarker for symptomatic genetic FTD carriers, with moderate accuracy to distinguish PPD from mild forms including C9orf72 . 3 key findings →
Participants: 474 Evidence: low
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Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers. 5 key findings →
Participants: 763 Evidence: low
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The claimed beneficial effects of the Mediterranean diet include prevention of several age-related dysfunctions including neurodegenerative diseases and Alzheimer-like pathology. 4 key findings →
Evidence: low
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• SCD patients showed attenuation of sensory (P1, N1, P2) and cognitive (P300, P600, P900) components, with performance-related gains. • MCI patients exhibited neural compensations, reversing the downward trend observed in SCD, which resulted in a non-monotonic pattern of ERPs. • The progression of cognitive decline was linked to electrophysiological discontinuity, suggesting resilience mechanisms in both low and higher order cognitive regions. 5 key findings →
Participants: 178 Evidence: moderate
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Subjective cognitive decline (SCD) is increasingly recognised as a potential preclinical stage of Alzheimer's disease, yet the physiological mechanisms underlying its progression remain poorly understood. 4 key findings →
Design: longitudinal study Evidence: moderate
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Lack of insight or impaired awareness of deficits in patients with dementia is a relatively neglected area of study. 4 key findings →
Participants: 37 Evidence: low
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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This study highlights the role of age, gender, APOE genotype, and depressive symptoms in the presentation and progression of cognitive decline. 2 key findings →
Evidence: moderate
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At baseline, MCI participants displayed elevated levels of IL-17A, CX3CL1, CCL11, with a borderline increase of IL-6 and TNFα. 5 key findings →
Participants: 76 Evidence: low
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This joint Position Paper, developed by the Italian Expert Panel on Alzheimer convened by the Italian Society of Neurology with participation from multiple scientific societies, outlines strategic guidelines for reorganizing the patient journey in the era of anti-amyloid monoclonal antibodies for Alzheimer's disease. 1 key finding →
Evidence: low
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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 →