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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1,351–1,375 of 1,380 studies in Disease mechanisms (page 55 of 56) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

What “Disease mechanisms” covers

Disease mechanisms — Cell- and molecule-level research into what actually goes wrong in Alzheimer's and related diseases.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

SpineTool 2.0: A Deep Learning Platform with an Interactive User Interface for Dendritic Spine Segmentation and Morphological Analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-21

Quantitative analysis of dendritic spine morphology is central to understanding synaptic function and its disruption in neurological disease, yet reliable measurement depends on accurate segmentation of spines from fluorescence microscopy images — a task still limited by faint or discontinuous spine necks and by tools that require extensive manual correction. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The Alzheimer’s disease risk gene ABCA7 regulates microglial lysosomal and lipid homeostasis and promotes phagocytosis to maintain neuronal health

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19

ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Stage-specific proteomic signatures of synaptopathy in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-03

Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood. 2 key findings →

Participants: 67 Evidence: low

Full summary, score breakdown and related studies → Original source

Long-term voluntary exercise reveals limited translation of hippocampal molecular responses into neuroprotection in 5xFAD mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24

Physical exercise promotes systemic and neural adaptations that support healthy brain aging and may mitigate Alzheimer’s disease (AD) progression. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Autonomous AI-Driven Nanoscale Spatial Mapping Reveals Novel Targets and Ternary Architectures in 5xFAD Alzheimer's Disease Model

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-16

Alzheimer's disease (AD) is characterized by the deposition of amyloid-beta (Aβ) and microtubule-associated protein tau (MAPT) neurofibrillary tangles in the brain; however, the molecular mechanisms underlying associated synaptic dysfunction remain unclear. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Discovery of Bavachin as a Dual Trk-A/Trk-B Agonist via Integrated Computational Screening and Experimental Validation

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-16

Neurotrophins regulate neuronal survival, differentiation, and synaptic plasticity through activation of tropomyosin receptor kinase (Trk) receptors, and their dysregulation is strongly implicated in neurodegenerative disorders, including Alzheimer’s disease. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Ion modulation restores local synaptic function in APOE4 neuronal networks despite persistent impairments in global network organization

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14

The apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD), which accounts for the vast majority of AD cases. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Soluble pathogenic tau transmission to astrocytes drives cellular senescence and neurovascular uncoupling in a model of Alzheimer’s tauopathy

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-12

Pathogenic tau oligomers are transmitted between neurons and non-neuronal cells and may contribute to cellular dysfunction in Alzheimer’s disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

BNIP3L/NIX-mediated mitophagy limits Alzheimer’s disease pathology and preserves neuronal function

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20

Defective mitophagy is emerging as a key contributor to Alzheimer’s disease (AD), but the neuronal pathways governing mitochondrial clearance and their contribution to disease progression remain poorly understood. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Spatiotemporal transcriptomic dynamic across the auditory pathway from young to old age in 5xFAD Alzheimer disease mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-18

Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Convergent Mitochondrial and Oxidative Stress Signatures in Spaceflight and Tauopathy: A Comparative Multi-Omics Reanalysis in Drosophila melanogaster

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19

Mitochondrial dysfunction is a shared biological thread between terrestrial Alzheimer’s disease (AD) and in the unique stress environment of spaceflight, making mitochondrial pathophysiology a compelling target for comparative investigation. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

PDE4D inhibition activates cAMP-PKA signaling to preserve mitochondrial homeostasis and prevent neuronal necroptosis in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12

Alzheimer’s disease involves progressive necroptosis of neurons, and the associated cognitive deficits can be mitigated by inhibiting cAMP-degrading phosphodiesterase 4D (PDE4D). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neuroprotective Effects and Mechanisms of Cannabinoids in In Vitro Cell Models of Neurodegenerative Diseases: A Scoping Review

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-13

Most included studies were purely in vitro (n = 18); six combined in vitro and in vivo methods, and two used in vitro and in silico or ex vivo components. 1 key finding →

Participants: 18 Evidence: low

Full summary, score breakdown and related studies → Original source

Integrative Multiomics Analysis Reveals a Coordinated Molecular Signature of Neuroresilience in human MAPT-knockout hiPSC-derived Neurons with relevance for Alzheimer’s and Neurodegenerative Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-14

These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Subtype-Selective Neuronal Vulnerability and Compensatory Neuroglial Remodeling in Human Cortical Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-11

Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

PDE2A Modulation Attenuates Aβ-Induced Neuronal Injury and Associated Oxidative, Inflammatory, and Apoptotic Responses

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-01

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

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Where “Free full text” comes from

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

How the 0–100 score works — and why some entries are capped

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.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

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 27,380 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.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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 →

Newest studies, as a dated timeline →    Atom feed