Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Across cellular and animal Aβ injury models, BML-288 attenuated oxidative and inflammatory disturbances, modulated apoptosis-related protein expression, and improved cognitive outcomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apigenin is an abundant, bioactive phytochemical with reported therapeutic potential and neuroprotective effects in a variety of age-related disease models. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurologic condition that is categorized by a progressive loss of neurons with time. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Environmental microplastics and nanoplastics (MNPs) are emerging contaminants that accumulate in human tissues, including the brain, yet their mechanistic impact on the nervous system remains poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although dementias primarily affect memory, they also disrupt our closest social relationships, resulting in elevated caregiver burden and worse patient outcomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The retina displayed earlier and broader AD-related molecular alterations than the hippocampus. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Machine learning (ML) methods have shown promise in modeling clinical trajectories associated with neurodegenerative disorders such as Alzheimer’s disease (AD). 3 key findings →
Design: longitudinal study Participants: 15,727 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Immunofluorescence staining of FFPE tissue following Xenium processing also preserves cellular morphology, allowing the morphological complexity of distinct cell types to be captured and quantitated, especially for glial cells with highly ramified processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The reproducibility crisis in biomedical research calls for re-evaluation of how common analytic approaches affect results. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Validated on synthetic ground truth, the audit separates a generalizable anchor (PTGDS) from a dataset-specific signal and a global-expression artefact, providing a reusable control for trajectory-based molecular staging. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
TAR DNA-binding protein 43 (TDP-43) is a key pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and a critical regulator of RNA splicing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMHs) are a hallmark of cerebral small vessel disease, commonly seen in cognitively normal older adults and patients with neurodegenerative disorders, and are thought to reflect varying degrees of tissue damage. 2 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) is a common cause of early-onset dementias marked by progressive declines in behavior, cognition, and/or movement. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adults with Down syndrome (DS) develop Alzheimer’s disease (AD) brain pathology by age 40 due to triplication of the Amyloid Precursor Protein ( APP ) gene on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques contain numerous proteins in addition to amyloid beta in Alzheimer’s disease (AD). 4 key findings →
Participants: 240 Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The integrated stress response (ISR) is a highly conserved network essential for maintaining cellular homeostasis and cognitive function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approximately 90% of Parkinson's disease (PD) patients exhibit olfactory deficits, which often precedes motor symptoms by years, and are a robust predictor for PD and subsequent cognitive decline. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurodegenerative processes underlying Alzheimer’s disease and related dementias (ADRD) begin years before clinical diagnosis, motivating scalable approaches for earlier identification. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings identify an anatomically specific age-related profile of the human BF, with structural vulnerability manifest and pre-diagnostic neurological disorders, which is not substantially explained by common inherited risk. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, and its incidence is rising rapidly with population aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 8,313 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
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 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 →