Basal ganglia calcification in BB/E rats with diabetes

• Published in: Journal of clinical neuroscience Vol. 12; no. 1; pp. 49 - 53
• Main Authors: Lammie, G.A.., Kelly, P.A.T., Baird, J.D., Smith, W., Chatterjee, S., Frier, B.M., Strachan, M.W.J.
• Format: Journal Article
• Language: English
• Published: Scotland Elsevier Ltd 2005
• Subjects: Actins - genetics; Actins - metabolism; Animals; Basal Ganglia - pathology; basal ganglia calcification; BB/E rats; Calcinosis - pathology; Cognition Disorders - etiology; diabetes mellitus; Diabetes Mellitus - genetics; Diabetes Mellitus - pathology; Diabetes Mellitus - psychology; Glial Fibrillary Acidic Protein - metabolism; Gliosis - pathology; Male; microangiopathy; Rats; microangiopathy; diabetes mellitus; BB/E rats; basal ganglia calcification
• ISSN: 0967-5868; 1532-2653
• DOI: 10.1016/j.jocn.2004.03.026

Human diabetes is associated with cognitive impairment and structural abnormalities in the brain such as cerebral atrophy. The aetiology of these abnormalities is not known. The BB/E rat is a well-established model of type 1 (insulin dependent) diabetes. A cohort of 34 BB/E rats with diabetes was divided into three sub-groups according to age (and duration of diabetes). Basal ganglia calcification (BGC) was present in the brains of more than 50% of diabetic animals, but not in any of 37 non-diabetic BB/E rats. BGC occurred more commonly in those animals which had the longest duration of diabetes (
p
=
0.001), such that BGC was present in only 8% of animals with diabetes for 20 weeks, but in 100% of animals with diabetes for 60 weeks. There were no other significant light microscopic neuropathologic changes in diabetic animals. It will be important to investigate the mechanism of brain calcification, whether a similar process occurs in humans with diabetes, and its possible relationship to cognitive decline.