Pathological aggregation of tau is a hallmark of Alzheimer’s disease and related tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Pathological aggregation of tau is a hallmark of Alzheimer’s disease and related tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ranolazine and metformin may be frequently co‐administered in subjects with chronic angina and co‐morbid type 2 diabetes mellitus (T2DM). 2 key findings →
Design: clinical trial Participants: 28 Evidence: low
Full summary, score breakdown and related studies → Original source
The dorsal PCC and retrosplenial cortex may have special importance in the pathogenesis and cognitive findings of AD. 5 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
The incidence of dementia and obstructive sleep apnea (OSA) increases with age. 2 key findings →
Evidence: low
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Vascular contributions to cognitive impairment are receiving heightened attention as potentially modifiable factors for dementias of later life. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Oxidative stress (OS) has been demonstrated to be involved in the pathogenesis of the two major types of dementia: Alzheimer's disease (AD) and vascular dementia (VaD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This review traces evidence that age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature. 2 key findings →
Evidence: low
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Effective communication by nursing home staff is related to a higher quality of life and a decrease in verbal and physical aggression and depression in nursing home residents. 2 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These data provide potential insights into the biology of CSF in AD and MCI progression and provide a novel tool for AD researchers and clinicians working to improve diagnostic accuracy, evaluation of treatment efficacy, and early diagnosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Growing evidence indicates that the activation of c-Jun N-terminal kinase (JNK) is implicated in the multiple major pathological features of Alzheimer disease (AD). 4 key findings →
Evidence: low
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According to the ' amyloid cascade hypothesis of Alzheimer's disease ' first proposed about 16 years ago, the accumulation of Aβ peptides in the human central nervous system (CNS) is the primary influence driving Alzheimer's disease (AD) pathogenesis, and Aβ peptide accretion is the result of an imbalance between Aβ peptide production and clearance. 2 key findings →
Evidence: low
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The triggering receptor expressed on myeloid cells (TREM) 2 is a member of the immunoglobulin superfamily of receptors and mediates signaling in immune cells via engagement of its co-receptor DNAX-activating protein of 12 kDa (DAP12). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Analyses of cerebrospinal fluid (CSF) biomarkers (β-amyloid protein, total tau protein, and hyperphosphorylated tau protein) are part of the diagnostic criteria of Alzheimer disease. 4 key findings →
Evidence: low
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Alzheimer's disease is a severe neurodegenerative disorder of the brain, pathologically characterized by extracellular beta-amyloid plaques, intraneuronal Tau inclusions, inflammation, reactive glial cells, vascular pathology and neuronal cell death. 1 key finding →
Evidence: low
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Attention deficit is one of the core symptoms of the attention-deficit/hyperactivity disorder (ADHD). 5 key findings →
Evidence: low
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Many insults, including trauma, ischemia, infection, inflammation, and neurodegeneration, result in irreversible damage to the central nervous system. 3 key findings →
Design: clinical trial Evidence: high
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Because of the growing size and aging of the world's population, the global burden of stroke is increasing dramatically. 2 key findings →
Evidence: low
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Bach1, among the genes encoded on chromosome 21, is a transcription repressor, which binds to antioxidant response elements of DNA thus inhibiting the transcription of specific genes involved in the cell stress response including heme oxygenase-1 (HO-1). 1 key finding →
Evidence: low
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Increasing evidence suggests that free radical-mediated oxidation of biological substrates is a key feature of Alzheimer's disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Decline in olfactory activity was correlated with the AD structural degeneration in the POC. 2 key findings →
Evidence: low
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The chemokine/chemokine receptor CCL2/CCR2 axis was impaired in BDMs from AD and MCI patients, causing a deficit in cell migration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Selecting a set of relevant markers to predict conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) has become a challenging task given the wealth of regional pathologic information that can be extracted from multimodal imaging data. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia prevalence increases with age and Alzheimer's disease (AD) accounts for up to 75% of cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synaptic disruption is an early pathological sign of the neurodegeneration of Dementia of the Alzheimer's type (DAT). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Relying on procedural memory is a promising approach for interventions that address the cognitive difficulties found in semantic dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →