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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 176–200 of 612 studies in Brain tissue and pathology (page 8 of 25) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these 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; 13,658 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.

The seeds of neurodegeneration: prion-like spreading in ALS

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Cell 2011-10-01

Misfolded proteins accumulating in several neurodegenerative diseases (including Alzheimer, Parkinson, and Huntington diseases) can cause aggregation of their native counterparts through a mechanism similar to the infectious prion protein's induction of a pathogenic conformation onto its cellular isoform. 2 key findings →

Evidence: low

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

Hippocampal sclerosis and TDP-43 pathology in aging and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Annals of neurology 2015-04-22

Diagnoses of dementia, probable AD, and MCI in 636 autopsied subjects from the Religious Order Study and the Rush Memory and Aging Project were based on clinical evaluation and cognitive performance tests. 4 key findings →

Evidence: low

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

Parkinson disease neuropathology: later-developing dementia and loss of the levodopa response

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Archives of neurology 2002-01-01

We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination. 4 key findings →

Participants: 13 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

A prospective 20-year longitudinal follow-up of dementia in persons with Down syndrome

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Journal of intellectual disability research : JIDR 2017-06-29

Goal To examine dementia characteristics, age at onset and associated co-morbidities in persons with Down syndrome. 4 key findings →

Participants: 77 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Oophorectomy, menopause, estrogen treatment, and cognitive aging: clinical evidence for a window of opportunity

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Brain research 2010-10-18

The neuroprotective effects of estrogen have been demonstrated consistently in cellular and animal studies but the evidence in women remains conflicted. 4 key findings →

Design: cohort study Evidence: moderate

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

APOE epsilon 4 lowers age at onset and is a high risk factor for Alzheimer's disease; a case control study from central Norway

✓ Peer-reviewed alzhub usefulness score 53 out of 100. BMC neurology 2008-04-16

The objective of this study was to analyze factors influencing the risk and timing of Alzheimer's disease (AD) in central Norway. 4 key findings →

Participants: 376 Evidence: low

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

FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Acta neuropathologica 2010-05-20

Through an international consortium, we have collected 37 tau- and TAR DNA-binding protein 43 (TDP-43)-negative frontotemporal lobar degeneration (FTLD) cases, and present here the first comprehensive analysis of these cases in terms of neuropathology, genetics, demographics and clinical data. 92% (34/37) had fused in sarcoma (FUS) protein pathology, indicating that FTLD-FUS is an important FTLD subtype. 4 key findings →

Evidence: low

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

Higher rates of decline for women and apolipoprotein E epsilon4 carriers

✓ Peer-reviewed alzhub usefulness score 53 out of 100. AJNR. American journal of neuroradiology 2013-07-04

Age and the apolipoprotein E ε4 allele are well-known risk factors for Alzheimer disease, but whether female sex is also a risk factor remains controversial. 4 key findings →

Design: longitudinal study Evidence: moderate

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

The Association Between Quantitative Measures of Dementia and of Senile Change in the Cerebral Grey Matter of Elderly Subjects

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The British Journal of Psychiatry 1968-07-01

The ageing of many populations in recent years has directed increasing attention to the social, medical and biological problems of senescence. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Where do you know what you know? The representation of semantic knowledge in the human brain

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature reviews. Neuroscience 2007-12-01

Mr M, a patient with semantic dementia--a neurodegenerative disease that is characterized by the gradual deterioration of semantic memory--was being driven through the countryside to visit a friend and was able to remind his wife where to turn along the not-recently-travelled route. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

A mutation in VPS35, encoding a subunit of the retromer complex, causes late-onset Parkinson disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. American journal of human genetics 2011-07-01

To identify rare causal variants in late-onset Parkinson disease (PD), we investigated an Austrian family with 16 affected individuals by exome sequencing. 4 key findings →

Evidence: low

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

Sleep, circadian rhythms, and the pathogenesis of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Experimental & molecular medicine 2015-03-13

Disturbances in the sleep-wake cycle and circadian rhythms are common symptoms of Alzheimer Disease (AD), and they have generally been considered as late consequences of the neurodegenerative processes. 4 key findings →

Evidence: low

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

Novel amyloid precursor protein mutation in an Iowa family with dementia and severe cerebral amyloid angiopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2001-06-01

Several mutations in the amyloid precursor protein (APP) gene have been found to associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

A stop-codon mutation in the BRI gene associated with familial British dementia

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature 1999-06-01

Familial British dementia (FBD), previously designated familial cerebral amyloid angiopathy-British type, is an autosomal dominant disorder of undetermined origin characterized by progressive dementia, spasticity, and cerebellar ataxia, with onset at around the fifth decade of life. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosis

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature neuroscience 2004-08-15

The E693Q mutation in the amyloid beta precursor protein (APP) leads to cerebral amyloid angiopathy (CAA), with recurrent cerebral hemorrhagic strokes and dementia. 4 key findings →

Evidence: low

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

Correlations between apolipoprotein E epsilon4 gene dose and brain-imaging measurements of regional hypometabolism

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2005-06-02

Patients with Alzheimer's disease (AD) have abnormally low positron emission tomography (PET) measurements of the cerebral metabolic rate for glucose (CMRgl) in regions of the precuneus and the posterior cingulate, parietotemporal, and frontal cortex. 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. 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 28,180 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.

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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →

Newest studies, as a dated timeline →    Atom feed