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Research

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

Find studies

Showing 126–150 of 290 studies in Brain tissue and pathology · free to read (page 6 of 12) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 290 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.

Adipokines: a link between obesity and dementia?

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Lancet. Neurology 2014-09-01

Being overweight or obese, as measured with body-mass index or central adiposity (waist circumference), and the trajectory of body-mass index over the life course have been associated with brain atrophy, white matter changes, disturbances of blood-brain barrier integrity, and risk of all-cause late-onset dementia and Alzheimer's disease. 4 key findings →

Evidence: low

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

TMEM106B, the risk gene for frontotemporal dementia, is regulated by the microRNA-132/212 cluster and affects progranulin pathways

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2012-08-01

Frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP) is a fatal neurodegenerative disease with no available treatments. 4 key findings →

Evidence: low

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

Molecular Pathological Classification of Neurodegenerative Diseases: Turning towards Precision Medicine

✓ Peer-reviewed alzhub usefulness score 51 out of 100. International journal of molecular sciences 2016-02-02

Neurodegenerative diseases (NDDs) are characterized by selective dysfunction and loss of neurons associated with pathologically altered proteins that deposit in the human brain but also in peripheral organs. 4 key findings →

Evidence: low

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

FUS pathology in basophilic inclusion body disease

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Acta neuropathologica 2009-10-15

Basophilic Inclusion Body Disease (BIBD) is a tau-negative form of frontotemporal lobar degeneration (FTLD), characterized by neuronal cytoplasmic inclusions (NCI) that are visible on hematoxylin and eosin stain (HE), contain RNA, and are inconsistently ubiquitin-immunoreactive (ir). 4 key findings →

Evidence: low

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

Cryptic splicing in synaptic and membrane excitability genes links TDP-43 loss to neuronal dysfunction

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Science Translational Medicine 2026-06-03

Using human stem cell-derived neurons, we show that TDP-43 reduction induces cryptic splicing and downregulation of these genes, resulting in impaired excitability and synaptic transmission. 1 key finding →

Evidence: low

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

Trajectories of general and central obesity beyond middle age in relation to late‐life cognitive decline and dementia

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Obesity 2025-01-28

General and central obesity trajectories beyond midlife with persistently high or increasing patterns were significantly associated with an increased risk of developing cognitive decline and dementia in late life. 3 key findings →

Design: longitudinal study Evidence: moderate

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

Serum neurofilament light is superior to glial fibrillary acidic protein to distinguish sporadic frontotemporal dementia from late-onset primary psychiatric disorders: a retrospective DIPPA-FTD study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. BMJ Neurology Open 2025-01-01

Significantly higher serum median NfL and GFAP levels were found in sporadic bvFTD (NfL 33.3 pg/mL, IQR (19.6-49.6); GFAP 124.5 pg/mL, IQR (83.5-181.6)) compared with PPD (NfL 12.2 pg/mL, IQR (9.8-17.9); GFAP 68.9 pg/mL, IQR (50.6-95.0), both p<0.001). 4 key findings →

Participants: 275 Evidence: moderate

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

High-Level Alzheimer Disease Neuropathological Change Following Iatrogenic Exposure

✓ Peer-reviewed alzhub usefulness score 51 out of 100. JAMA Neurology 2026-03-30

The study describes 4 males who developed dementia following confirmed or suspected c-hGH treatment in childhood (age at symptom onset between 47 and 60 years) with cognitive syndromes characterized by prominent language involvement. 4 key findings →

Participants: 14 Evidence: low

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

Plasma TAR DNA-binding protein 43 (TDP-43) levels in a population-based cohort of older adults: The cardiovascular health study

✓ Peer-reviewed alzhub usefulness score 51 out of 100. Journal of Alzheimer s Disease 2025-04-23

Brain deposition of transactive response DNA-binding protein 43 (TDP-43) is a feature of neurodegenerative syndromes. 1 key finding →

Design: cross-sectional Participants: 1,058 Evidence: moderate

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

Brain-derived neurotrophic factor is associated with age-related decline in hippocampal volume

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2010-04-01

Hippocampal volume shrinks in late adulthood, but the neuromolecular factors that trigger hippocampal decay in aging humans remains a matter of speculation. 4 key findings →

Evidence: low

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

Enrichment of C-terminal fragments in TAR DNA-binding protein-43 cytoplasmic inclusions in brain but not in spinal cord of frontotemporal lobar degeneration and amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The American journal of pathology 2008-06-05

TAR DNA-binding protein (TDP-43) has been recently described as a major pathological protein in both frontotemporal dementia with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis. 4 key findings →

Evidence: low

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

A decamer duplication in the 3' region of the BRI gene originates an amyloid peptide that is associated with dementia in a Danish kindred

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2000-04-01

Familial Danish dementia (FDD), also known as heredopathia ophthalmo-oto-encephalica, is an autosomal dominant disorder characterized by cataracts, deafness, progressive ataxia, and dementia. 4 key findings →

Evidence: low

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

TDP-43 pathology in Alzheimer's disease, dementia with Lewy bodies and ageing

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Brain pathology (Zurich, Switzerland) 2016-08-24

Intracellular inclusions consisting of TAR DNA binding protein-43 (TDP-43 pathology) are present in up to 57% of Alzheimer's disease (AD) cases and follow a distinct topographical pattern of progression described in the TDP-43 in AD staging scheme. 4 key findings →

Evidence: low

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

Associations of Lifetime Cognitive Enrichment With Incident Alzheimer Disease Dementia, Cognitive Aging, and Cognitive Resilience

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2026-02-11

= 0.02). Lifetime exposure to cognitive enrichment was related to lower risk of AD dementia and a slower rate of cognitive decline, including after adjustment for common ADRD pathologies, indicating higher resilience provided by lifetime enrichment. 2 key findings →

Design: longitudinal study Evidence: moderate

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

TDP-43 in the ubiquitin pathology of frontotemporal dementia with VCP gene mutations

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neuropathology and experimental neurology 2007-02-01

Frontotemporal dementia with inclusion body myopathy and Paget disease of bone is a rare, autosomal-dominant disorder caused by mutations in the gene valosin-containing protein (VCP). 4 key findings →

Evidence: low

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

Repetitive mild brain trauma accelerates Abeta deposition, lipid peroxidation, and cognitive impairment in a transgenic mouse model of Alzheimer amyloidosis

✓ Peer-reviewed alzhub usefulness score 49 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2002-01-01

Traumatic brain injury (TBI) increases susceptibility to Alzheimer's disease (AD), but it is not known how TBI contributes to the onset or progression of this common late life dementia. 4 key findings →

Participants: 15 Evidence: low

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

PARylation regulates stress granule dynamics, phase separation, and neurotoxicity of disease-related RNA-binding proteins

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Cell research 2019-02-06

Mutations in RNA-binding proteins (RBPs) localized in ribonucleoprotein (RNP) granules, such as hnRNP A1 and TDP-43, promote aberrant protein aggregation, which is a pathological hallmark of various neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 4 key findings →

Evidence: low

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

TDP-43 accumulation in inclusion body myopathy muscle suggests a common pathogenic mechanism with frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of neurology, neurosurgery, and psychiatry 2008-10-01

TAR DNA binding protein-43 (TDP-43) is found in ubiquitinated inclusions (UBIs) in some frontotemporal dementias (FTD-U). 4 key findings →

Evidence: low

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

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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.

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