Both patient groups showed significant deviations from HC, but with distinct patterns. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Both patient groups showed significant deviations from HC, but with distinct patterns. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The Cronbach alpha coefficient of the RUDAS scale is 0.8529. 5 key findings →
Participants: 87 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Surprisingly, demographic normalisation worsened rather than improved diagnostic accuracy for detecting MCI with both MoCA and MMSE, reducing their effectiveness as diagnostic tools and confirming our hypothesis. 5 key findings →
Evidence: low
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CAA may be encountered as an isolated pathology or with Alzheimer disease and has been demonstrated to be associated with an increased risk of seizures. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment. 1 key finding →
Evidence: low
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Cerebral amyloid angiopathy (CAA), which is prevalent among older adults, constitutes a major cause of brain hemorrhage, dementia, and cognitive decline. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Acute and chronic treatment of JRMS reduced TDP-25 aggregation in a dose-dependent manner by ∼75% in cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aβ treatment inhibited microglial activity and phagocytosis, but SMOC2 disruption enhanced these functions (p < 0.05). 4 key findings →
Evidence: low
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Astrocytes are a source of IL-15 in AD, particularly near localized Aβ pathology, and neurons are poised to respond. 3 key findings →
Evidence: low
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We demonstrate that irisin promotes the expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), glial cell line-derived neurotrophic factor (GDNF), α5 subunits of integrin receptors and LDH5α, and stimulates transient activation of ERK 1/2 in astrocytes. 3 key findings →
Evidence: low
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We found that induction of adult human brain-like 4R Tau isoform expression enables endogenous formation of late-stage Tauopathy hallmarks in iPSC-derived neurons engineered to contain synergistic Tau mutations. 5 key findings →
Evidence: low
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Barnes Maze Acquisition was performed on males (N = 4-5/genotype) after habituation and several days training. 5 key findings →
Evidence: low
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The basal nucleus showed significant neuronal loss in PPA versus controls (p <0.05). 5 key findings →
Evidence: low
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PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8). 5 key findings →
Evidence: low
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PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8). 5 key findings →
Evidence: low
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Alzheimer's disease (AD), the most common form of dementia, is characterized by progressive cognitive decline and neuropathological hallmarks, including amyloid-beta plaques and tau tangles. 1 key finding →
Evidence: low
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Neurogranin levels were significantly reduced in MTLE-HS patients as compared to FLE patients and healthy controls but were not correlated with any of the clinical and cognitive variables. 5 key findings →
Participants: 51 Evidence: low
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Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive memory loss and cognitive decline. 1 key finding →
Evidence: low
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This study aims to investigate how cognitive impairment and social presence influence goal attainment in an ecological virtual environment. 2 key findings →
Evidence: low
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Mild cognitive impairment (MCI) is the transitional stage between normal cognition and dementia and is associated with arterial stiffness, which may lead to cardiovascular disease. 4 key findings →
Evidence: low
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Current evidence suggests a potential for the Mediterranean diet to prevent cognitive decline, largely supported by observational studies, although randomized controlled trials show mixed results. 1 key finding →
Evidence: high
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The moral authority of advance directives (ADs) in the context of persons living with dementia (PLWD) has sparked a multifaceted debate, encompassing concerns such as authenticity and the appropriate involvement of caregivers. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to investigate the association between delirium and incident dementia in elderly (≥65 years) type 2 diabetes mellitus (T2DM) patients, addressing the heightened dementia risk in this population. newly diagnosed between January 1, 2005, and December 31, 2007. 2 key findings →
Evidence: low
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The prevalence of dysphagia in Aotearoa New Zealand is estimated to have been approximately 1.78% in 2020, with the biggest aetiological contributors being stroke, Alzheimer's disease and other dementias, and gastroesophageal reflux disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Between April 2020 and March 2021, the number of fall-related emergency admissions in England for adults over 65 years was 1933 per 100 000 people. 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 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 →