ArticlePloS one2023
AA-amyloidosis in cats (Felis catus) housed in shelters.
Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Epigallocatechin-3-Gallate: A potential amyloid Fibril Disaggregator of Serum amyloid A1.Biochemistry and biophysics reports · 2025Article
- High prevalence of renal amyloidosis in cats in an overcrowded colony.The Journal of veterinary medical science · 2025Article
- Polymorphisms in SAA alter intrarenal amyloid distribution of AA amyloidosis in cats.Scientific reports · 2025Article
- Histological evaluation of the distribution of systemic AA-amyloidosis in nine domestic shorthair cats.PloS one · 2023Article
- Cryo-EM structure of ex vivo fibrils associated with extreme AA amyloidosis prevalence in a cat shelter.Nature communications · 2022Article
- Renal amyloid-A amyloidosis in cats: Characterization of proteinuria and biomarker discovery, and associations with kidney histology.Journal of veterinary internal medicineArticle
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Authors and funding
24 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic AA-amyloidosis is a protein-misfolding disease characterized by fibril deposition of serum amyloid-A protein (SAA) in several organs in humans and many animal species. Fibril deposits originate from abnormally high serum levels of SAA during chronic inflammation. A high prevalence of AA-amyloidosis has been reported in captive cheetahs and a horizontal transmission has been proposed. In domestic cats, AA-amyloidosis has been mainly described in predisposed breeds but only rarely reported in domestic short-hair cats. Aims of the study were to determine AA-amyloidosis prevalence in dead shelter cats. Liver, kidney, spleen and bile were collected at death in cats from 3 shelters. AA-amyloidosis was scored. Shedding of amyloid fibrils was investigated with western blot in bile and scored. Descriptive statistics were calculated. In the three shelters investigated, prevalence of AA-amyloidosis was 57.1% (16/28 cats), 73.0% (19/26) and 52.0% (13/25), respectively. In 72.9% of cats (35 in total) three organs were affected concurrently. Histopathology and immunofluorescence of post-mortem extracted deposits identified SAA as the major protein source. The duration of stay in the shelters was positively associated with a histological score of AA-amyloidosis (B = 0.026, CI95% = 0.007-0.046; p = 0.010). AA-amyloidosis was very frequent in shelter cats. Presence of SAA fragments in bile secretions raises the possibility of fecal-oral transmission of the disease. In conclusion, AA-amyloidosis was very frequent in shelter cats and those staying longer had more deposits. The cat may represent a natural model of AA-amyloidosis.
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