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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 58 studies in Brain tissue and pathology published 2026 (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 58 studies, in this order: BibTeX (.bib) · RIS (.ris)

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; 16,851 studies have no institution on record and are not counted here.

What “Brain tissue and pathology” covers

Brain tissue and pathology — What is found in the brain itself, usually after death: plaques, tangles and other changes, and how they match symptoms in life.

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.

Elucidation of Molecular Mechanisms of Lipid-Altered Cytotoxicity of TDP-43 Fibrils

✓ Peer-reviewed alzhub usefulness score 38 out of 100. ACS Chemical Neuroscience 2026-01-29

Progressive aggregation of TAR DNA-binding protein 43 (TDP-43) is a hallmark of numerous neurodegenerative diseases, including amyotrophic lateral sclerosis, frontotemporal dementia, Alzheimer's disease, and limbic predominant age-related TDP-43 encephalopathy (LATE). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Small molecule JRMS modulating importin-β1 chaperone activity as a therapeutic strategy reducing TDP-43 pathology

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neurotherapeutics 2026-01-01

Neuronal cytoplasmic aggregation and nuclear depletion of the TAR DNA-binding protein 43 (TDP-43) is the most characteristic pathology of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), causing toxicity through cytoplasmic gain and nuclear loss of function mechanisms. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Chemical and Molecular Strategies in Restoring Autophagic Flux in TDP-43 Proteinopathy

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecules 2026-03-10

The cytoplasmic accumulation of TDP-43 aggregates remains a persistent pathological hallmark of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43 encephalopathy (LATE). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

From Evasion to Collapse: The Kinetic Cascade of TDP-43 and the Failure of Proteostasis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. International Journal of Molecular Sciences 2026-01-23

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases that, despite the availability of symptomatic and modestly beneficial treatments, still lack therapies capable of halting disease progression. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TDP-43 pathology triggers neuroinflammation and cognitive impairment by inducing microglial necroptosis

✓ Peer-reviewed alzhub usefulness score 36 out of 100. EMBO Molecular Medicine 2026-03-10

Pathological TAR DNA-binding protein-43 (TDP-43) is a defining feature of several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer's disease (AD). 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Detecting Self-Repairs from Spontaneous Speech with Prompt Ablation Across LLMs and Fine-Tuned Encoder

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-25

Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Context Matters in LLM-Assisted Qualitative Data Analysis: Workflow Development and Multidimensional Evaluation in Health Research

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-11

Large language models (LLMs) are increasingly used for qualitative analysis, but strong language performance does not guarantee strong interpretation when meaning depends on method and context. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Distinct lipid mediator profiles in brain and liver tissues in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-23

INTRODUCTIONInflammation plays a central role in Alzheimers Disease (AD), with oxylipins, endocannabinoids, and polyunsaturated fatty acids (PUFAs) acting as potent modulators. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Inflammatory biomarker candidates in dementia with Lewy bodies: diagnostic classification, clinical associations, and survival

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-11-01

Dementia with Lewy bodies (DLB) is a common neurodegenerative dementia that remains difficult to distinguish clinically from Alzheimer's disease (AD) and related disorders because of overlapping clinical features and frequent mixed pathology. 4 key findings →

Participants: 20 Evidence: low

Full summary, score breakdown and related studies → Original source

Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27

VU0155069 engages circuit- and pathological stage-specific forms of dendritic spine remodeling across distributed recognition- and associative-memory networks. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A coordinated and reproducible multicellular response to AD pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-23

While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A brain immune phenotype independent of Alzheimer’s Disease associates with amyloid susceptibility and systemic inflammation

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

Transcriptomic and proteomic studies have consistently demonstrated substantial molecular heterogeneity across patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, leading to the proposal of multiple disease subtypes. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Systematic identification of perioperative neurocognitive disorder related biomarkers in Alzheimer’s disease and development of machine learning-based diagnostic models

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

Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations. 5 key findings →

Evidence: moderate

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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events