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Research

30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 1–21 of 21 studies in Brain tissue and pathology with an author at University of California, San Francisco (US) · 30,980 in the whole library · How the 0–100 score works

Download bibliography of these 21 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.

Other institutions

From OpenAlex; 16,452 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.

Large-scale plasma proteomic analysis identifies proteins and pathways associated with dementia risk

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature aging 2021-05-14

The plasma proteomic changes that precede the onset of dementia could yield insights into disease biology and highlight new biomarkers and avenues for intervention. 4 key findings →

Participants: 4,110 Evidence: moderate

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

An acetylated Tau-174 CSF biomarker discriminates between TDP-43 and tau pathology in patients with frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Nature Medicine 2026-04-15

Biomarkers to determine underlying frontotemporal lobar degeneration (FTLD) tau or TAR DNA-binding protein (TDP) pathology during life are needed to advance clinical trials targeting specific FTD pathologies. 3 key findings →

Participants: 513 Evidence: moderate

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

Amyloid deposition, hypometabolism, and longitudinal cognitive decline

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Annals of neurology 2012-10-01

Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) population, we examined (1) cross-sectional relationships between amyloid deposition, hypometabolism, and cognition, and (2) associations between amyloid and hypometabolism measurements and longitudinal cognitive measurements. 4 key findings →

Design: cross-sectional Evidence: moderate

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

High complement levels in astrocyte-derived exosomes of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Annals of neurology 2018-03-10

Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →

Participants: 28 Evidence: low

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

Neuropathological basis of magnetic resonance images in aging and dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2008-01-01

Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →

Participants: 93 Evidence: moderate

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

Timing of hormone therapy and dementia: the critical window theory revisited

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2010-11-12

Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →

Participants: 1,524 Evidence: low

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

Association of brain amyloid-β with cerebral perfusion and structure in Alzheimer's disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Brain : a journal of neurology 2014-03-12

Patients with Alzheimer's disease have reduced cerebral blood flow measured by arterial spin labelling magnetic resonance imaging, but it is unclear how this is related to amyloid-β pathology. 4 key findings →

Participants: 51 Evidence: low

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

Proteomics-based aging clocks in midlife or late-life and their associated risk of dementia

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Communications Medicine 2025-08-14

We investigated whether a discrepancy between chronological and biological age in midlife and late-life is associated with cognition and dementia risk. 5 key findings →

Design: cohort study Participants: 11,758 Evidence: moderate

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

Cerebrospinal fluid tau and amyloid-β1-42 in patients with dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Brain : a journal of neurology 2015-06-30

Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease. 4 key findings →

Evidence: moderate

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

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

Small-Molecule Modulation of TDP-43 Recruitment to Stress Granules Prevents Persistent TDP-43 Accumulation in ALS/FTD

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neuron 2019-07-01

Stress granules (SGs) form during cellular stress and are implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis and frontotemporal dementia (ALS/FTD). 4 key findings →

Evidence: low

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

Heritability for Alzheimer's disease: the study of dementia in Swedish twins

✓ Peer-reviewed alzhub usefulness score 51 out of 100. The journals of gerontology. Series A, Biological sciences and medical sciences 1997-03-01

Alzheimer's disease has been thought to have familial and sporadic forms, and several genetic defects have been identified that chiefly explain early-onset familial cases. 4 key findings →

Evidence: low

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

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

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

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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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.

1,040 records (3.4% of the library) are not peer-reviewed — 965 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