30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study presents the Edinburgh Cognitive and Behavioural ALS Screen (ECAS), developed for ALS patients with physical disability for use by health care professionals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The increasing prevalence of cognitive impairment among the older adult population warrants attention to the identification of practices that may minimize the progression of early forms of cognitive impairment, including the transitional stage of mild cognitive impairment (MCI), to permanent stages of dementia. 3 key findings →
Evidence: low
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Awareness of palliative care as an option for patients with COPD needs to increase in palliative care services, physicians and the general public. 1 key finding →
Evidence: low
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Advances in automatic text classification have been necessitated by the rapid increase in the availability of digital documents. 5 key findings →
Participants: 21 Evidence: low
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Alzheimer disease (AD) results, in part, from the excess accumulation of the amyloid-β (Aβ) peptide as neuritic plaques in the brain. 4 key findings →
Evidence: low
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Perturbation of lipid metabolism favours progression of Alzheimer disease, in which processing of Amyloid Precursor Protein (APP) has important implications. 4 key findings →
Evidence: low
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γ-Secretase is an intramembrane aspartyl protease that cleaves the amyloid precursor protein to produce neurotoxic β-amyloid peptides (i.e. Aβ42) that have been implicated in the pathogenesis of Alzheimer disease. 4 key findings →
Evidence: low
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Neurofibrillary tangles, one of the hallmarks of Alzheimer disease (AD), are composed of paired helical filaments of abnormally hyperphosphorylated tau. 4 key findings →
Evidence: low
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The University of Minnesota Medical School in Minneapolis, Minnesota, and the Salhgrenska University Hospital, Sweden. 4 key findings →
Evidence: low
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Current evidence suggests a central role for autophagy in Alzheimer disease (AD), and dysfunction in the autophagic system may lead to amyloid-β (Aβ) accumulation. 4 key findings →
Evidence: low
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Many trials of drugs aimed at preventing or clearing β-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms. 4 key findings →
Design: clinical trial Evidence: low
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The association between an AD-like signature using the established biomarkers Aβ42, T-tau, and P-tau with increased levels of NFL provides in vivo evidence of an association between AD and subcortical axonal degeneration in this uniquely large dataset of CSF samples tested for dementia biomarkers. 2 key findings →
Evidence: low
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There is considerable interest in designing therapeutic studies of individuals at risk of Alzheimer disease (AD) to prevent the onset of symptoms. 4 key findings →
Evidence: low
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Accumulation of β-amyloid (Aβ) in the brain is a key event in Alzheimer disease pathogenesis. 3 key findings →
Evidence: low
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Significantly increased levels of oxidized nucleic acids, proteins, and lipids have been described in the brains of subjects with Alzheimer disease (AD) and mild cognitive impairment (MCI) as well as young adults with Down syndrome, compared to age-matched controls. 2 key findings →
Design: randomized controlled trial Evidence: high
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Loss of cognitive function is one the most devastating manifestations of ageing and vascular disease. 1 key finding →
Evidence: low
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The results suggest that it is possible to automatically quantify the task quality of smart home activities and perform limited assessment of the cognitive health of individual if smart home activities are properly chosen and learning algorithms are appropriately trained. 3 key findings →
Participants: 263 Evidence: low
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There is increasing use of neuroimaging modalities, including PET, for diagnosing dementia. 5 key findings →
Evidence: low
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Late-onset Alzheimer's disease (LOAD), which is characterized by progressive deterioration in cognition, function, and behavior, is the most common cause of dementia and the sixth leading cause of all deaths, placing a considerable burden on Western societies. 2 key findings →
Evidence: low
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Hearing loss has been linked to many types of cognitive decline in adults, including an association between hearing loss severity and dementia. 4 key findings →
Evidence: low
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Frontotemporal lobar degeneration (FTLD) can manifest as a spectrum of clinical syndromes, ranging from behavioural impairment to language or motor dysfunction. 1 key finding →
Evidence: low
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In normal adult brain the microtubule associated protein (MAP) tau contains 2-3 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein. 5 key findings →
Evidence: low
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Genetic deficits and loss of function for the triggering receptor expressed in myeloid cells 2 (TREM2; encoded at chr6p21.1), a transmembrane spanning stimulatory receptor of the immunoglobulin/lectin-like gene superfamily, have been associated with deficiencies in phagocytosis and the innate immune system in Alzheimer's disease. 4 key findings →
Evidence: low
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MicroRNA (miR) dysregulation is found in Alzheimer disease (AD). 4 key findings →
Evidence: low
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γ-Secretase generates amyloid β-protein (Aβ), a pathogenic molecule in Alzheimer disease, through the intramembrane cleavage of the β-carboxyl-terminal fragment (βCTF) of β-amyloid precursor protein. 4 key findings →
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.
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 →