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Research

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

Find studies

Showing 1–25 of 36 studies in Brain pathology (Zurich, Switzerland) (page 1 of 2) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 36 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.

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.

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.

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

TREM2 expression in the human brain: a marker of monocyte recruitment?

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain pathology (Zurich, Switzerland) 2017-10-30

Mutation in the triggering receptor expressed on myeloid cells (TREM) 2 gene has been identified as a risk factor for several neurodegenerative diseases including Alzheimer's disease (AD). 4 key findings →

Participants: 299 Evidence: low

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

The cerebral beta-amyloid angiopathies: hereditary and sporadic

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain pathology (Zurich, Switzerland) 2006-01-01

We review the clinical, radiologic, and neuropathologic features of the hereditary and sporadic forms of cerebral amyloid angiopathy (CAA) associated with vascular deposition of the beta-amyloid peptide. 4 key findings →

Evidence: low

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

White matter changes in dementia: role of impaired drainage of interstitial fluid

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2015-01-01

White matter abnormalities on magnetic resonance imaging (MRI) are associated with dementia and include white matter hyperintensities (WMH; also termed leukoaraiosis) and visible perivascular spaces (PVS). 2 key findings →

Evidence: low

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

TREM2 Protein Expression Changes Correlate with Alzheimer's Disease Neurodegenerative Pathologies in Post-Mortem Temporal Cortices

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2014-11-11

Triggering receptor expressed by myeloid cells 2 (TREM2), a member of the immunoglobulin superfamily, has anti-inflammatory phagocytic function in myeloid cells. 4 key findings →

Evidence: low

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

TREM2-induced activation of microglia contributes to synaptic integrity in cognitively intact aged individuals with Alzheimer's neuropathology

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2022-07-11

The existence of individuals who remain cognitively intact despite presenting histopathological signs of Alzheimer's disease (AD), here referred to as "Nondemented with AD neuropathology" (NDAN), suggests that some mechanisms are triggered to resist cognitive impairment. 4 key findings →

Evidence: low

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

Variability in the type and layer distribution of cortical Aβ pathology in familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain pathology (Zurich, Switzerland) 2021-07-28

Familial Alzheimer's disease (FAD) is caused by autosomal dominant mutations in the PSEN1, PSEN2 or APP genes, giving rise to considerable clinical and pathological heterogeneity in FAD. 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source

Human brain parenchymal microglia express CD14 and CD45 and are productively infected by HIV-1 in HIV-1 encephalitis

✓ Peer-reviewed alzhub usefulness score 42 out of 100. Brain pathology (Zurich, Switzerland) 2002-10-01

Microglia are endogenous brain macrophages that show distinct phenotypes such as expression of myeloid antigens, ramified morphology, and presence within the neural parenchyma. 4 key findings →

Evidence: low

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

Evidence of beta amyloid independent small vessel disease in familial Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Brain pathology (Zurich, Switzerland) 2022-06-13

We studied small vessel disease (SVD) pathology in Familial Alzheimer's disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer's disease (SAD) as a positive control for Alzheimer's pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Geniposide ameliorates learning memory deficits, reduces tau phosphorylation and decreases apoptosis via GSK3β pathway in streptozotocin-induced alzheimer rat model

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Brain pathology (Zurich, Switzerland) 2014-02-12

Intracerebral-ventricular (ICV) injection of streptozotocin (STZ) induces an insulin-resistant brain state that may underlie the neural pathogenesis of sporadic Alzheimer disease (AD). 4 key findings →

Evidence: low

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

A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain pathology (Zurich, Switzerland) 2003-10-01

Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. 4 key findings →

Evidence: low

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

Considerations for integrative multi-omic approaches to explore Alzheimer's disease mechanisms

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain pathology (Zurich, Switzerland) 2020-09

The past decade has seen the maturation of multiple different forms of high-dimensional molecular profiling to the point that these methods could be deployed in initially hundreds and more recently thousands of human samples. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Inflammasome activation and innate immunity in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain pathology (Zurich, Switzerland) 2017-03

Activation of innate immunity and the assembly of microglial cells at sites of Alzheimer disease pathology has long been regarded as bystander phenomenon, which does not actively contribute to disease pathogenesis and progression. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Synaptic actin stabilization protein loss in Down syndrome and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Brain pathology (Zurich, Switzerland) 2019-09-08

Reduced spine densities and age-dependent accumulation of amyloid β and tau pathology are shared features of Down syndrome (DS) and Alzheimer's disease (AD). 3 key findings →

Evidence: low

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

Iron accumulation in microglia triggers a cascade of events that leads to altered metabolism and compromised function in APP/PS1 mice

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Brain pathology (Zurich, Switzerland) 2019-02-17

Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function and iron accumulation. 4 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 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