2026-01-05 ノースカロライナ州立大学(NC State)
<関連情報>
- https://news.ncsu.edu/2026/01/researchers-develop-guidelines-for-diagnosing-monitoring-canine-cognitive-decline/
- https://avmajournals.avma.org/view/journals/javma/aop/javma.25.10.0668/javma.25.10.0668.xml
犬認知機能障害症候群ワーキンググループによる犬認知機能障害症候群の診断とモニタリングに関するガイドライン The Canine Cognitive Dysfunction Syndrome Working Group guidelines for diagnosis and monitoring of canine cognitive dysfunction syndrome
Natasha J. Olby VetMB, PhD, DACVIM,Joseph A. Araujo BSc,Margaret E. Gruen DVM, PhD, DACVB,Phillipa Johnson BVSc, MSc, DECVDI,Eniko Kubinyi PhD,Gary Landsberg DVM, DACVB,Caitlin S. Latimer MD, PhD,Stephanie McGrath DVM, DACVIM,Brennen McKenzie VMD,Julie A. Moreno PhD,Monica Tarantino DVM, andHolger Volk DVM, PhD, DECVN,…
Journal of the American Veterinary Medical Association Published:24 Dec 2025
DOI:https://doi.org/10.2460/javma.25.10.0668
Abstract
Canine cognitive dysfunction syndrome (CCDS) is diagnosed with increasing frequency, yet standardized diagnostic guidelines are lacking. The CCDS Working Group, an international group combining experts in the field and primary care veterinarians, proposes a definition of the syndrome and practical diagnostic criteria designed to aid clinicians and researchers alike. Canine cognitive dysfunction syndrome is defined as a chronic, progressive, age-associated neurodegenerative syndrome, characterized by cognitive and behavioral changes that affect daily life to varying degrees. These changes affect the behavioral domains of disorientation, social interaction, sleep disruption, house soiling, learning and memory, activity changes, and anxiety (DISHAA). We propose 3 severity stages. In mild CCDS, signs are subtle and of low frequency or severity, with preserved function. With progression, behavioral changes become more apparent and impactful, requiring management adjustments. In severe CCDS, debilitating deficits are overt, significantly impairing basic functions and necessitating comprehensive support. Two diagnostic levels are proposed. Level 1 is based on consistent history of progressive DISHAA signs, identification of alternate causes through physical, orthopedic, and neurologic examination and laboratory work; either normal neurologic examination or evidence of symmetrical, diffuse forebrain dysfunction; and persistence of signs following management of relevant comorbidities. Level 2 includes a brain MRI showing cortical atrophy with CSF cell counts within normal limits. Definitive postmortem histopathological confirmation rests on cortical atrophy, amyloid deposition, myelin loss, neuroinflammation, and amyloid angiopathy. Future priorities include the development of blood biomarkers and cognitive testing batteries for routine clinical settings, both of which will refine diagnostic accuracy and therapeutic monitoring.
