Plasma β-amyloid peptides in canine aging and cognitive dysfunction as a model of Alzheimer's disease

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• 作者：Á ; ngela Gonzá ; lez-Mart&#xed ; nez^a ; ¹ ; Belé ; n Rosado^b ; ¹ ; Pedro Pesini^c ; ^{pedropesini@araclon.com"" rel=""nofollow} ; Mar&#xed ; a-Luisa Suá ; rez^a ; Germá ; n Santamarina^a ; Sylvia Garc&#xed ; a– ; Belenguer^b ; Ainara Villegas^b ; Inmaculada Monleó ; n^c ; Manuel Sarasa^c
• 关键词：Amyloid-beta protein ; Plasma ; Alzheimer's disease ; Animal behavior ; Canine ; ELISA ; Neurodegeneration ; Brain aging
• 刊名：Experimental Gerontology
• 出版年：2011
• 出版时间：July 2011
• 年：2011
• 卷：46
• 期：7
• 页码：590-596
• 全文大小：374 K

文摘

Aging dogs naturally demonstrate cognitive impairment and neuropathology that model early Alzheimer's disease (AD). In particular, there is evidence that canine cognitive dysfunction syndrome (CDS) in aged dogs is accompanied by cortical deposition of Aβ peptides and neurodegeneration. Plasma Aβ levels have been examined in humans as putative biomarkers for AD, but to date, no similar studies have been conducted for canine dementia. The aim of the present study was to assess plasma Aβ1-42 and Aβ1-40 levels in a blind study using pet dogs that were either successfully aging or exhibiting CDS. The severity of cognitive impairment was assessed using an owner-based questionnaire. On average, young dogs presented significantly higher plasma levels of Aβ1-42 and Aβ1-40 than aged, cognitively unimpaired dogs. Notably, among aged dogs, the levels of Aβ1-42 and the Aβ42/40 ratio were significantly higher in those showing mild cognitive impairment than in either cognitively unimpaired or severely affected dogs. These results suggest that increased plasma Aβ1-42 levels and Aβ42/40 ratio could be a biomarker for canine cognitive dysfunction, which is considered an excellent natural model of early AD.