OMIA:000038-37347 : Amyloidosis, AA in Tupaia belangeri (northern tree shrew)

In other species: chicken , bats , white-tufted-ear marmoset , dog , red fox , domestic cat , Sumatran tiger , bottlenosed dolphin , pig , taurine cattle , goat , sheep , cheetah , Japanese squirrel , zebra finch , island gray fox

Categories: Homeostasis / metabolism phene

Links to MONDO diseases: No links.

Mendelian trait/disorder: unknown

Considered a defect: yes

Cross-species summary: “Amyloid is the term for a misfolded protein that accumulates as insoluble fibrils in various organ and tissue sites to result in a clinical syndrome known as amyloidosis. The chemical diversity of amyloid and amyloidosis has been evident since the mid-1970s and the number of known human amyloid proteins has steadily increased from two at that time to 36 at Amyloid deposition, either hereditary or acquired, is seldom benign and, when clinical symptoms appear, they are frequently life-threatening. The best way to distinguish the different forms of amyloid is by chemical characterization. (Immuno-)histochemical typing of amyloid is readily available … . [A] second descriptor is whether the patient’s amyloid is limited (localized) or throughout the whole body (systemic). Each amyloid syndrome should be named according to the Nomenclature Guidelines of the ISA. Most of the distinct amyloidosis syndromes are named after the fibril forming protein, e.g. AL (amyloid derived from immunoglobulin light chain) amyloidosis (localized or systemic), AA amyloidosis (amyloid derived from SAA – serum amyloid A protein) … .” (International Society of Amyloidosis) Sipe et al., 2016: “The terms “hereditary amyloidosis” and “familial amyloidosis” refer to different entities. The term “hereditary amyloidosis” should be used when there is a mutation in the fibril protein gene itself, e.g. ATTR, ALys or AFib. The term “familial amyloidosis” should be used when the syndrome occurs in a familial setting due to mutations in genes expressing non-amyloid proteins, e.g. AA amyloidosis.”

Species-specific description: Klein et al. (2022): "A high prevalence of AA-amyloidosis was identified in a breeding colony of northern tree shrews (Tupaia belangeri) ... The lack of distinctive predisposing factors suggests a general susceptibility of captive T. belangeri to develop amyloidosis."

Genetic engineering: Unknown
Have human generated variants been created, e.g. through genetic engineering and gene editing

Cite this entry

Nicholas, F. W., Tammen, I., & Sydney Informatics Hub. (2023). OMIA:000038-37347: Online Mendelian Inheritance in Animals (OMIA) [dataset]. https://omia.org/. https://doi.org/10.25910/2AMR-PV70

Reference

2022 Klein, A., Radespiel, U., Felmy, F., Brezina, T., Ciurkiewicz, M., Schmitz, J., Bräsen, J.H., Linke, R.P., Reinartz, S., Distl, O., Beineke, A. :
AA-amyloidosis in captive northern tree shrews (<i>Tupaia belangeri</i>). Vet Pathol 59:340-347, 2022. Pubmed reference: 34931557. DOI: 10.1177/03009858211066847.

Edit History


  • Created by Imke Tammen2 on 09 Jan 2022
  • Changed by Imke Tammen2 on 16 Jan 2023