P. 560

An Urban Experience
B. Blicher Thomsen1
1University of Copenhagen, Department of Veterinary Clinical Sciences, Frederiksberg C, Denmark
Trine Schütt, DVM, PhD1
Barbara Blicher Thomsen, DVM, PhD2
1. LEO Pharma, Industriparken 55, DK-2750 Ballerup. E-mail:
2. University of Copenhagen, Dyrlaegevej 16, DK-1870 Frederiksberg C. E-mail:
Clinical phenotype
Canine cognitive dysfunction (CCD) is an age-related neurodegenerative condition characterised by a progressive decline in cognitive functioning, which
is clinically expressed as changes in certain learned behaviors and daily routines. Similarities to the early stages of human Alzheimer´s disease (AD) have been found in relation to both the clinical course and to
some pathological  ndings. Consequently, synonyms
of CCD include canine counterpart of senile dementia
of the Alzheimer’s type, canine dementia, and canine dysfunction syndrome. The prevalence of CCD ranges from 14 to 35% in dogs more than eight years of age and the risk of developing CCD increases exponentially with increasing age. Thus, age is considered as the most important risk factor. It has been found that a diagnosis of CCD does not affect survival compared to healthy aging control dogs. The clinical phenotype of CCD is characterised by a slowly progression of speci c behavioural alterations such as aimless wandering/ pacing, staring into space, decreased social interaction, house-soiling, and disturbances in the sleep-wake cycle. Additionally, signs of fear and anxiety that have not been present earlier and dif culty in  nding dropped food have also been reported as common signs for dogs suffering from CCD. Clinical signs of the cognitive decline are cumulative and will worsen over time.
Diagnostic work-up and associated challenges
Obtaining a  nal diagnosis of CCD can only be done via a post-mortem brain biopsy. Thus, in affected dogs the optimal diagnostic approach is to exclude systemic and intracranial diseases mimicking the clinical signs related to CCD. Common differential diagnoses include brain tumors, endocrine and metabolic disorders, chronic
pain conditions, or vision/hearing loss. When excluding differential diagnoses relevant investigations should include a thorough clinical and neurological examination plus para-clinical tests such as a complete blood
count, serum biochemistry, thyroid pro le, urinalysis, magnetic resonance imaging (MRI) of the neurocranium, and possibly cerebrospinal  uid analysis. Obtaining a detailed history focusing on signs that may be associated with CCD is essential. Several owner-based screening questionnaires exist, and these may prove very useful when evaluating a dog with suspected CCD. An obstacle, however, is that there that there is a great variability between these questionnaires with respect to design and scoring method. Other complicating issues are that no systematic international consensus on the evaluation criteria for establishing an ante-mortem diagnosis of CCD exists. Additionally, cognitive tasks which appropriately measures decline in cognitive abilities, memory, and spontaneous activity in companion dogs are still in development and are not yet applicable in a clinical setting.
Therapeutic interventions
As for humans suffering from AD, there is presently no cure for CCD. Selegiline, also known as L-deprenyl,
is the only drug which in some countries has been approved for CCD. This drug may have a symptomatic effect by slowing down the cognitive decline in some dogs. Preventive approaches, such as supplement of antioxidants, L-carnitine or omega-3 fatty acids may have a bene cial effect in some dogs. Mental stimulation, such as training and playing, and keeping daily routines may help in maintaining a good quality of life. Finally, adjunctive therapy targeting the speci c clinical signs is considered key when managing dogs that present in the clinic with signs compatible with CCD.
Neuropathology in the aging canine brain
Examples of neurodegenerative changes that have been identi ed in the aging dog brain includes neuronal loss and thereby cortical atrophy, oxidative damage, dysfunction in the neurotransmitter systems, plus deposition of amyloid-beta (Aβ) protein as extracellular plaques in the cerebral cortex and in the walls of both parenchymal and meningeal vessels. The amino acid sequence of canine Aβ peptide is identical to the human sequence. However, plaques have only been found to be of the diffuse type and not as neuritic plaques which can be found in the aging human brain. As in human
AD research, the majority of focus has been on the association between quanti cation of the Aβ plaque load and degree of cognitive impairment. Results and conclusions from these studies vary as all studies can demonstrate a positive correlation between plaque

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