Prevention of cognitive changes in the senior dog patient

CANINE COGNITIVE DYSFUNCTION
Dr. Jill Cline
Research Nutritionist
Nestle Purina PetCare
More and more dogs seen in practice are of the older, more mature variety than ever
before. Mirroring the human population, the average age of dogs in developed
countries has increased- over 25% of dogs in Europe are considered senior. Also
mirroring the human population, increased age in dogs results in increased
degenerative changes in organ systems like the cardiovascular, musculoskeletal,
endocrine and renal systems. Over the past two decades, behaviourists physiologists
and veterinarians agree that there are measurable and defined changes in brain
function in dogs associated with age.
Whilst some level of cognitive decline is a normal part of the aging process, Canine
Cognitive Dysfunction (CCD) is not. CCD is caused by well defined pathological
changes.
Definitions
Cognition is defined as the mental processes such as perception, learning, memory,
awareness and decision making which allow the dog to take in information, process
and retain that information and make decisions based on that information.
CCD is a breakdown in these cognitive abilities. It is also known as Senile Dementia
or “doggy Alzheimer’s” although its pathology is not the same as Alzheimer’s disease
in humans
Epidemiology
A recent study Neilson et al examined the cognition of 180 senior dogs aged 11 to 16
years old. The dogs were split into 3 groups based on their age (11-12 years. 13- 14
years and 15- 16 years) and four categories of cognition were assessed:
Impairment in any one category was defined as the dog exhibiting 2 clinical signs in
that category. Mild CCD was defined as the dog exhibiting abnormalities in only 1
category. Severe CCD was defined as the dog exhibiting abnormalities in 2 or more
categories. (Figure 1). The study also showed that most dogs showed progression in
their disease over a 6- 18 month period.

Clinical Signs of Canine Cognitive Dysfunction
The initial clinical signs of CCD are often mild with gradual progression. For this
reason it is very easy to miss in the early stages unless vets ask specific appropriate
questions when taking a history from the owner of a senior dog. It is vital to include a
behavioural questionnaire in all geriatric consultations to allow early diagnosis and
prompt intervention.
Behavioural changes in senior dogs with cognitive impairment can be classified into 5
general categories:
The 5 categories of Cognitive Impairment in Dogs:
1. disorientation in the home or garden 2. changes in social interactions with human family members 3. loss of house training 4. changes in the sleep wake cycle 5. altered activity levels
The first 3 categories clearly reflect losses of memory and learning. Changes in the
sleep- wake cycle would appear to reflect disruption in the normal circadian rhythm;
however, wild dogs usually show a crepuscular pattern of activity (active at dusk and
dawn) and adaptation to the diurnal pattern of humans by domestic canines probably
also represents a type of learning which can be lost with cognitive impairment.
Diagnosis of CCD
A diagnosis of CCD is usually a tentative one based on the dog exhibiting appropriate
clinical signs and ruling out all other causes of the cognitive impairment. It is
absolutely vital to rule out medical conditions first as each of the clinical signs of
CCD can be caused by medical conditions which obviously need to be treated
completely differently to CCD. It must be born in mind however that senior dogs may
have medical conditions and CCD concurrently.
Differential Diagnoses of CCD
The following does not provide an exhaustive list but gives suggestions as to
conditions which can cause the same clinical signs as CCD and which therefore must
be ruled out before a diagnosis of CCD can be made:
1. Disorientation • Sensory deficits (hearing and/ or vision loss) • Neurological disease (e.g. tumours) • Cardiovascular disease 2. Change in social interactions (loss of cognition and recognition) • Sensory deficits (hearing and/ or vision loss) • Pain 3. Loss of housetraining • Gastrointestinal disease • Urinary tract disease • Endocrine disease if causing polydipsia and polyuria 4. Sleep wake cycle disturbances • Sensory deficits (hearing and/ or vision loss) • Pain 5. Altered activity levels • Arthritis • Pain • Cardiovascular disease Other general differential diagnoses which can cause many of the same clinical signs as CCD include encephalitis, Central Nervous System tumours and metabolic conditions such as hypothyroidism.
Pathology
Old dogs do not get Alzheimer’s disease because they do not have the same
neuropathology. There are similarities though as dogs with CCD are found to have ß
amyloid protein (senile plaques) in the cortical regions of their brain which correlate
with clinical signs. Dogs with CCD also show reduced cerebral blood flow, reduced
dopamine levels in the brain, increased levels of free radicals leading to cellular injury
and decreased glucose metabolism by neurons.
Dog vs Human Pathological Changes

Change Associated with
Cognitive Dysfunction Βeta-amyloid plaques metabolism in the brain Decreased frontal lobe volume
Human Dementia
Human dementia is diagnosed when cognitive deficits exceed what is expected for
the age of the person and when they are severe enough to compromise a person’s
social and/ or occupational functioning. It is diagnosed when a person has
significant memory impairment plus at least one of the following:
• Agnosia (failure to recognise people) • Apraxia (reduced purposeful movement) • Disturbed executive function (ability to plan, organise or pay attention) Many times, canine patients exhibit behaviours which mirror the human symptoms of agnosia, apraxia and disturbed executive function.
Treatment
The only drug licensed to treat CCD is Selegiline Hydrochloride (L Deprenyl) which
is a selective and irreversible inhibitor of monoamine oxidase B (MAO B). Selegiline
has immune-system boosting and anti- neurodegenerative effects. It acts in four main
ways:
• It increases dopamine concentrations and metabolism • It reduces the levels of substances in the brain responsible for glial cell • It protects nerve cells from oxidative stress (free radical damage) and • It promotes synthesis of nerve growth factors
Therapeutic effects of selegiline are thought to result in part from enhanced
catecholaminergic nerve function and increased dopamine levels in the CNS. The
pathogenesis of the development of clinical signs associated with cognitive decline is
considered to be partly a result of a decrease in the level of catecholamines in the
CNS and deficiencies in neurotransmission. Selegiline can take up to 3-6 weeks to
work.
Other drugs which can be considered include Nicergoline and Propentofylline. Both
these drugs help improve cerebral blood flow by promoting cerebral vasodilation and
have some neuroprotective properties.
A combination of selegiline and propentofylline may provide the best results.
2. Nutrition
When considering how to improve memory, learning and trainability of dogs with CCD, there are three specific areas of nutrition to consider: a. Antioxidants have been shown to reduce neuropathology and promote
recovery in neurons exhibiting signs of neuropathology. They act by combating free radicals and reducing oxidative damage
b. Caloric restriction- Limiting caloric intake can slow the rate of a dog’s
cognitive decline in old age. Why this works has not been fully elucidated but nevertheless it is wise to advise owners of senior dogs (and indeed dogs of all ages) to limit their food intake to maintain an optimal body condition score. c. Medium Chain Triglycerides (MCTs) have proven to be the breakthrough
o Increase energy sources available for starving brain neurons o Ameliorate the effects of compromised glucose metabolism in the The benefits of this innovative intervention are: • Improved memory in senior dogs • Increased attention span and ability to learn • Increased interactivity between senior dogs and their environment including the owner and other household members MCTs are readily metabolised into beta hydroxybutyrate (BHB) and acetoacetate and released into the circulation and where they are used by extrahepatic tissues such as the brain as an energy source. One contributing factor to CCD is glucose malabsorption and utilization. The provision of increased quantities of ketone bodies to the aging brain provides an alternative energy source to the neurons at a time when glucose supply and utilisation is impaired. 3. Mental stimulation and behavioural support
Dogs with CCD benefit hugely from the provision of mental stimulation and
behavioural support from their owners. Immense patience and understanding are
required because these dogs often need to relearn common tasks such as
housetraining. The key to success is to supply structure and predictability,
consistent messages, simple commands and clear rewards. Any training or
stimulation should be given in short bursts as dogs with CCD have a limited
concentration span.
Whilst aging is an inevitability which all dog owners recognise, it can be very
distressing when a faithful member of the family develops the clinical signs of
CCD. Detecting this condition at the earliest opportunity will enable these dogs to
receive the best advice and veterinary care to help ameliorate the symptoms and
provide an enhanced quality and quantity of life. Incorporating a programme to
detect CCD cases early on and implement appropriate management including
nutritional intervention will vastly improve the care given to geriatrics by
veterinary practices.
References/ Further Reading

1. Bain MJ, Hart BL, Cliff KD, Ruehl WW. Predicting behavioural changes associated with cognitive impairment in dogs. JAVMA 2001; 218 (11) 1792- 1795 2. Chapman BL and Voith VL. Behavioural problems in old dogs 26 cases (1984- 3. Cummings BJ, Head E, Afagh AJ, Milgram NW, Cotman CW. Beta amyloid accumulation correlates with cognitive dysfunction in the ages canine. Neurobiology of Learning and Memory 1996; 66: 11- 23 4. Hart BL, Neilson JC, Ruehl WW. Behavioural Changes in Ageing Dogs: A demographic analysis. In: Mills DS, Heath SE, Harrington LJ. Proceedings of the First International Conference on Veterinary Behavioural Medicine 1997: 31- 33 5. Kitani K, Kanai S, Ivy GO, Carillo MC. Assessing the effects of deprenyl on longevity and antioxidant defences in different animal models. Ann NY Acad Sci 1998; 854: 291- 306 6. Neilson JC, Hart BL, Cliff KD, Ruehl WW. Prevalence of behavioural changes associated with age- related cognitive impairment in dogs. JAVMA 2002; 218 (11): 1787- 1791 7. Penalligon J. The use of nicergoline in the reversal of behaviour changes due to aging in dogs: a multi-centre clinical field. In: Mills DS, Heath SE, Harrington LJ. Proceedings of the First International Conference on Veterinary Behavioural Medicine 1997: 37- 41 8. Reger MA, Henderson ST, Hale C et al. Effects of β-hydroxybutyrate on cognition in memory impaired adults. Neurobiology of Aging 2004; 25 : 311-314 9. Tapp PD, Siwak CT, Gao, FQ. Frontal lobe volume , function and β-amyloid pathology in a canine model of aging. J Neuroscience 2004; 24: 8205-8213

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