In this study, altered AQP4 expression was associated with aging brains. 4 key findings →
Participants: 79 Evidence: low
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27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this study, altered AQP4 expression was associated with aging brains. 4 key findings →
Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Prevalent hemodialysis patients demonstrate significant cognitive decline, particularly within tests of executive function. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal lobar degeneration (FTD), Lewy body disease (LBD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have in common that protein aggregates represent pathological hallmark lesions. 1 key finding →
Evidence: low
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Sequence variations in the triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to an increased risk for neurodegenerative disorders such as Alzheimer's disease and frontotemporal lobar degeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolomics identified key disease-related metabolic changes and disease-progression-related changes. 1 key finding →
Evidence: low
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Neuroimaging has made it possible to measure pathological brain changes associated with Alzheimer's disease (AD) in vivo. 2 key findings →
Evidence: low
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Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) were recently found to increase the risk for developing Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in APP, PSEN1, and PSEN2 lead to early-onset Alzheimer disease (EOAD) but account for only approximately 11% of EOAD overall, leaving most of the genetic risk for the most severe form of Alzheimer disease unexplained. 4 key findings →
Design: case-control study Evidence: moderate
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Sleep disturbance is common in dementia, although it is unclear whether differences in sleep architecture precede dementia onset. 4 key findings →
Evidence: low
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Cardiometabolic diseases (hypertension, coronary artery disease [CAD] and diabetes are known to associate with poorer cognitive ability but there are limited data on whether having more than one of these conditions is associated with additive effects. 4 key findings →
Participants: 474 Evidence: moderate
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Residents' QoL was negatively associated with advanced dementia, PDU, and NPS. 5 key findings →
Design: cross-sectional Participants: 207 Evidence: low
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Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) is a progressive degenerative white matter disorder. 1 key finding →
Design: systematic review Evidence: high
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The UK Biobank cohort is a population-based cohort of 500,000 participants recruited in the United Kingdom (UK) between 2006 and 2010.
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Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer's disease (AD).
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MCI diagnosis usually was associated with comorbid neuropathologies; less than one-quarter of MCI cases showed "pure" AD at autopsy. 1 key finding →
Participants: 1,337 Evidence: low
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The findings suggest that detection of αSyn oligomers by αSyn-PMCA in the CSF of patients affected by PD may offer a good opportunity for a sensitive and specific biochemical diagnosis of the disease. 5 key findings →
Participants: 76 Evidence: moderate
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Semantic-lexical retrieval and lexical search may represent distinct aspects of semantic memory. 1 key finding →
Evidence: high
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Cerebrovascular disease typically manifests with stroke, cognitive impairment, or both. 2 key findings →
Evidence: low
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An increased HV:CTV ratio was predictive of faster clinical decline in participants with AD who were clinically indistinguishable at baseline except for a greater dysexecutive presentation. 1 key finding →
Participants: 229 Evidence: low
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Variation in use of APMs in U.S. nursing homes based upon facility characteristics exemplifies the need for a more systematic protocol guiding the use of these medications, along with heightened regulatory policies and enforcement. 2 key findings →
Design: meta-analysis Evidence: high
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Exposure to particulate matter (PM) in the ambient air and its interactions with APOE alleles may contribute to the acceleration of brain aging and the pathogenesis of Alzheimer's disease (AD). 1 key finding →
Evidence: moderate
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These models have revealed insights into frontotemporal dementia, Huntington's disease, multiple sclerosis, Parkinson's disease and other conditions. 4 key findings →
Design: longitudinal study Evidence: moderate
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TDP-43 is a primarily nuclear RNA-binding protein, whose abnormal phosphorylation and cytoplasmic aggregation characterizes affected neurons in patients with amyotrophic lateral sclerosis and frontotemporal dementia. 3 key findings →
Evidence: low
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Neuroinflammation is an important contributor to Alzheimer's disease (AD) pathogenesis, as underscored by the recent identification of immune-related genetic risk factors for AD, including coding variants in the gene TREM2 (triggering receptor expressed on myeloid cells 2). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Montreal Cognitive Assessment (MoCA) has a high sensitivity for detecting cognitive dysfunction. 4 key findings →
Participants: 758 Evidence: moderate
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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 →