By Dr Liesel van der Merwe
This short article attempts to summarise the most salient and practical aspects of the oxidative stress in the body and what mechanisms the body employs to minimise manage it.
Oxidative stress is a by-product of daily metabolic functions which enable living. The majority of complex life on earth requires oxygen for its existence but oxygen is also a highly reactive molecule that damages living organisms by producing reactive oxygen species. Inflammatory disease, ageing, congestive heart failure CHF, liver disease, stress, cancer, exercise can all increase oxidative stress. It is often unclear if oxidants trigger the disease, or if they are produced as a secondary consequence of the disease.
Changes associated with ageing may be physiological (changes in body composition, metabolic rates and special senses) or pathological. Several recommendations for alterations in nutrient intake in older dogs have been made.
|Several recommendation for alterations in nutrient intake in older dogs (and cats)|
|Energy||Increase / decrease||Senior dogs have overall decreased energy requirements but older dogs are also more likely to be underweight.|
|Protein||Increased – unless there is evidence of disease requiring protein reduction||Protein requirements of older dogs increase with age because of increased protein turnover. In cats protein absorption is decreased.|
|Fat||Increased or decreased||Senior dogs should have no alteration in fat digestibility with age.|
|Long chain W3 fatty acids||No alterations/ increase||Inconclusive evidence but long chain fatty acids may be beneficial in delaying the onset and progression of several physiological ageing processes|
|Anti-oxidants||No alterations or increase||Inconclusive evidence but studies indicate that dietary enrichment wih a variety of anti-oxidant combinations improves cognitive function.|
Organisms contain a complex network of antioxidant metabolites and enzymes that work together to prevent oxidative damage to cellular components such as DNA, proteins and lipids. In general, antioxidant systems either prevent these reactive species from being formed, or remove them before they can damage vital components of the cell. These oxidants can damage cells by starting chemical chain reactions such as lipid peroxidation, or by oxidizing DNA or proteins. Damage to DNA can cause mutations and possibly cancer, if not reversed by DNA repair mechanisms, while damage to proteins causes enzyme inhibition, denaturation and protein degradation.
Antioxidants are substances which have the ability to scavenge (ROS) and reduce the overall number of oxidants in a system. It is now accepted that the various antioxidant mechanisms in a system act synergistically. The major anti-oxidant systems in the body in include the enzymatic anti-oxidants superoxide dismutase (SAD), catalase and glutathione peroxidase, and the oxidant consumers which include Vitamin C, Vitamin E, glutathione and beta-carotene. The function of anti-oxidant systems is not to remove oxidants entirely, but instead to keep them at an optimum level as radical oxygen species (ROS) do have some positive functions.
Antioxidants are classified into two broad divisions, depending on whether they are soluble in water (hydrophilic) or in lipids (lipophilic). In general, water-soluble antioxidants react with oxidants in the cell cytosol and the blood plasma, while lipid-soluble antioxidants protect cell membranes from lipid peroxidation. See table 1
|Ascorbic acid (vitamin C)||Water|
|α-Tocopherol (vitamin E)||Lipid|
|Ubiquinol (coenzyme Q)||Lipid|
Some compounds contribute to antioxidant defence by chelating metals and preventing them from catalysing the production of free radicals in the cell. Of special importance is the ability to sequester iron, which is the function of iron-binding proteins such as transferrin and ferritin. The trace elements selenium and zinc are commonly referred to as antioxidant nutrients, but these chemical elements have no anti-oxidant action themselves and are instead required for the activity of some antioxidant enzymes.
Although certain levels of antioxidant vitamins in the diet are required for good health, there is considerable debate on whether anti-oxidant rich foods or supplements have anti-disease activity. Moreover, if they are actually beneficial, it is unknown which antioxidant(s) / combinations thereof are needed from the diet and in what amounts beyond typical dietary intake.
In order to critically evaluate the therapeutic potential for antioxidants (and other nutraceuticals) for the aging process is to consider the outcome measures used to determine efficacy. A variety of new laboratory methods have been developed to try to measure the effects of ROS in biologic systems the potential results of an intervention. Markers are specific for different biomolecules such as DNA (8-oxodeoxyguanosine), lipids (alkenals, MDA, TBARS), prostaglandins (isoprostanes) protein (nitrotyrosine, protein carbonyls), and advanced glycation endproducts (AGE). Some associations have been made between reduction of these markers of oxidative damage and improved health outcomes.
Supplementation and efficacy cannot be extrapolated from human studies. The selection of compounds, dosage range, length of administration, and route of administration may vary considerably across species. The selection of specific compounds may depend on bioavailability and supplementation with antioxidants may, or may not, increase absorption into tissues. Many have species or meal variation differences in absorption.
Vitamin C, a redox catalyst, is maintained in its reduced form by reaction with glutathione and can reduce, and thereby neutralize, reactive oxygen species such as hydrogen peroxide. Vitamin C is found in high concentrations in fruits. It can be synthesized in the canine liver but cannot be stored. Its production is decreased in chronic liver disease. Most commercial pet foods contain sufficient amounts of vitamin C and supplementation should only be required for malabsorption syndromes (EPI) and where extra anti-oxidant activity is required (cognitive dysfunction).
Vitamin E is a fat soluble vitamin found in high concentrations in nuts and oils. Vitamin E is the collective name for a set of eight related tocopherols and tocotrienols, which are fat soluble vitamins.
Alpha-tocopherol is the most widespread form of Vitamin E in animal foods and organisms. It is the form with the greatest bioavailability and biological anti-oxidant activity, with the body preferentially absorbing and metabolising this form. It protects membranes from oxidation by reacting with lipid radicals produced in the lipid peroxidation chain reaction which removes the free radical intermediates and prevents the propagation reaction. The oxidised α-tocopheroxyl radicals produced that can be recycled back to the active reduced form through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol (Co-enzyme Q10).
Flavonols are anti-oxidants found in plants and are the most important plant pigments for flower colouration, producing yellow or red/blue pigmentation. Animals significant quantities in their diet. Foods with a high flavonoid content include parsley, onions, blueberries and other berries, black tea, green tea and oolong tea, bananas, all citrus fruits, Ginkgo biloba, red wine, sea-buckthorns, buckwheat, and dark chocolate (with a cocoa content of 70% or greater).
Sstudies indicate that flavonoids may affect anti-inflammatory mechanisms due to their ability to inhibit reactive oxygen or nitrogen compounds. Flavonoids have also been proposed to inhibit the pro-inflammatory activity of enzymes involved in free radical production, such as cyclo-oxygenase, lipo-oxygenase or inducible nitric oxide synthase.
Carotenoids are organic pigments which are produced by plants and algae, as well as several bacteria and fungi. Compounds are deeply coloured yellow, orange, or red. Carotenoids from the diet are stored in the fatty tissues of animals, and exclusively carnivorous animals obtain the compounds from animal fat. There are over 600 known carotenoids; they are split into two classes, xanthophylls (which contain oxygen) and carotenes (which are purely hydrocarbons, and contain no oxygen). Humans and animals are mostly incapable of synthesizing carotenoids, and must obtain them through their diet. Dogs absorb beta carotene differently from humans, cleaving it and leaving very little intact b-carotene. In part, the beneficial effects of carotenoids are thought to be due to their role as antioxidants. b-carotene may have added benefits due its ability to be converted to vitamin A.
S-adenosylmethionine (SAMe) is a precursor of glutathione, a major antioxidant molecule in the body. Oral supplementation can assist to replenish glutathione stores. In addition SAMe also has anti-inflammatory properties.
Glutathione is an important antioxidant in animals and is capable of preventing damage to important cellular components caused by reactive oxygen species such as free radicals, peroxides, lipid peroxides and heavy metals.
Glutathione reduces disulfide bonds formed within cytoplasmic proteins to cysteines by serving as an electron donor. In the process, glutathione is converted to its oxidized form, glutathione disulfide (GSSG). Once oxidized, glutathione can be reduced back by glutathione reductase, using NADPH as an electron donor. (Note: a very important antioxidant in haemoglobin – especially feline haemoglobin , due to the increased number of sulphide bonds in this species.)
Glutathione exists in both reduced (GSH) and oxidized (GSSG) states. In the reduced state, the thiol group of cysteine is able to donate a reducing equivalent (H++ e−) to other molecules, such as reactive oxygen species to neutralize them. After donating an electron, glutathione itself becomes reactive and readily reacts with another reactive glutathione to form glutathione disulfide (GSSG). Such a reaction is probable due to the relatively high concentration of glutathione in cells. GSH can be regenerated from GSSG by the enzyme glutathione reductase. In healthy cells and tissue, more than 90% of the total glutathione pool is in the reduced form (GSH) and less than 10% exists in the disulfide form (GSSG).
The ratio of reduced glutathione to oxidized glutathione within cells is often used as a measure of cellular oxidative stress.
Melatonin is a strong antioxidant which easily crosses cell membranes and the blood–brain barrier. Unlike other antioxidants, melatonin does not undergo redox cycling, which is the ability of a molecule to undergo repeated reduction and oxidation. Redox cycling may allow other antioxidants (such as vitamin C) to act as pro-oxidants and promote free radical formation. Melatonin, once oxidized, cannot be reduced to its former state because it forms several stable end-products upon reacting with free radicals. Therefore, it has been referred to as a terminal (or suicidal) antioxidant.
Recent research has shown that some molecules classified as mitochondrial co-factors (lipoic acid, L-carnitine) may also act to enhance function of aged mitochondrion such that there are less ROS produced during aerobic respiration. Supplementation of foods with these co-factors increases their concentration within cells restores mitochondrial efficiency and reduces oxidative damage to RNA.
L-carnitine is an amino acid synthesised in the liver and kidney from lysine and methionine in the presence of ascorbate. L-carnitine facilitates the transportation of long chain fatty acids into the mitochondria where they undergo b–oxidation which produces a large amount of energy (ATP).The main dietary sources of carnitine are red meat, fish and dairy products. White meat is less rich in L-carnitine and vegetables contain none. Because L-carnitine can be synthesised de novo – it is not considered an essential nutrient.
Co-enzyme Q10 is a co-factor required for energy production and has anti-oxidant properties. It is a fat-soluble substance, which resembles a vitamin, and is present primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, which generates energy in the form of ATP. Ninety-five percent of the human body‘s energy is generated this way. Therefore, those organs with the highest energy requirements—such as the heart, liver, and kidney—have the highest CoQ10 concentrations.
The take home message here is that nutraceutical supplementation of anti-oxidants is a very INEXACT science. One cannot just buy a single supplement from a health shop and start supplementing. There seems to be an important interaction between the different types of anti-oxidants for maximum effect . More publications assessing the oxidative stress of various disease processes in animals and the results of interventions are coming out in the literature in recent years.
Cognitive Dysfunction in Geriatric Dogs and Cats
Canine cognitive dysfunction is a neurodegenerative disease very similar to Alzheimers in humans . It is characterised by a gradual onset of cognitive decline over a prolonged period (18 – 24 months).
The acronym DISHAAL has been used to describe the categories of clinical signs shown:
D – Disorientation (spatial disorientation and confusion, increased anxiety or restlessness)
I – Interactions are altered (decrease perception or responsiveness)
S – Sleep-Wake cycle alterations (night waking)
H – House soiling (altered learning and memory)
A – Activity level altered (purposeless, repetitive or decreased activity)
A – Anxiety (vocalisation/fear)
L – Learning and memory
Not all senior dogs develop cognitive deterioration and in most they are mild but some pets do develop overt cognitive dysfunction syndrome. Owners of affected pets often find it increasingly difficult to cope with the changes in their pets’ behaviour and the human-animal bond can be stressed or broken. Many owners will need to make painful decisions based upon both their own and their pets’ quality of life.
A study showed that 28% of owners of dogs 10 – 11 years old report at least one sign of cognitive change but this increases to 68% of owners of 15 – 16 year old dogs. In pets which are trained – such as guide dogs and working dogs – dysfunction may detected at an earlier age. The most commonly reported signs of cognitive dysfunction in dogs is aimless pacing and wandering and staring blankly (91%) and avoiding being patted and difficulty finding dropped food (75%).
The typical age of onset of presentation of cognitive decline in pets is traditionally set at about 11 years of age, based on owner reports. When data from laboratory animals studied with standardised assessment tools are evaluated however, the decline is noted to start at about seven years of age. This discrepancy emphasises the insidious nature of the change.
Owners do not usually present their animals to their veterinarian vet for cognitive dysfunction as they assume the changes are just unavoidable ageing. It is thus imperative that veterinarians are proactive in asking questions regarding changes in behaviour during a consultation and also in educating their clients in this condition. In a marketing study by Hills Pet Nutrition, 75% of owners of dogs aged 7 years and older reported at least one change in behaviour consistent with cognitive dysfunction but only 12% of these owners had reported the change to their veterinarian of their own accord.
Brain Function and Ageing
With increasing age there is a reduction in brain mass, increased ventricular size, meningeal calcification, demyelination and glial changes, neuro-axonal degeneration and a reduction in neurons. In dogs, cats and human beings with cognitive dysfunction there is also an increased accumulation of diffuse beta -amyloid plaques and perivascular infiltrates. In humans neurofibrillar tangle formation is an important component of the disease. This is not seen in dogs but is seen in cats. Cerebral arteriorsclerosis may also be seen in older dogs and cats resulting in compromised blood flow. Changes are irreversible but clinical signs can be managed and improved.
The brain is highly metabolically active, accounting for 2-3% of body weight yet consuming 25% of available glucose. Normally glucose is the main energy source of the brain. Cerebral glucose metabolism is reduced in healthy ageing people and dogs. Cerebral glucose metabolism correlates strongly with cognitive function and reduced metabolism occurs years before clinical signs are evident.
With ageing there is an increase in reactive oxygen species leading to oxidative damage. The brain may be particularly susceptible of the effects of free radicals because of its high lipid content, high rate of oxidative metabolism and limited ability for regeneration. Functional changes in the ageing brain include depletion of monoamine oxidase inhibitors (MAOIs) and a decline in cholinergic activity. Increases in MAO activity increases dopamine catabolism and also increases free radicals. Widespread oxidative damages , free radical production and lowered Vitamin E levels have all been demonstrated in dogs with dementia
Ketone bodies (KB) can be used as an alternative energy source for the brain when available;–prolonged starvation, and high fat- low carbohydrate diets. KB can supply up to 60% of the energy requirements of the brain during starvation in humans.
Collectively these ageing changes cause working memory dysfunction as well as alterations in motor function and REM sleep.
The most central diagnostic tool for detecting CCD is owner-based (Tables 1 and 2).
|Cognitive Dysfunction Screening Test|
|Age first noticed||Score: mild, moderate , severe|
|Confusion – awareness – spatial orientation|
|– Gets stuck or cannot get around objects|
|– Stares blankly at floors or walls|
|– Decreased recognition of familiar objects or people|
|– Goes into wrong side of doors/ walks into doors / walls|
|Relationships – social interactions|
|– Decreased in patting / avoids contact|
|– Decreased greeting behaviour|
|– Overdependent/ clingy|
|– Altered relationship with other pets – less contact|
|– Altered relationship with other pet – anxiety, fear|
|– Aggression – family members / unfamiliar people|
|– Aggressions – family pets / others|
|Response to stimuli|
|– Decreased response to auditory stimuli (sound)|
|– Increased response (fear / anxiety) to auditory stimuli|
|– Decreased response to visual stimuli|
|– Increased response (fear/anxiety) to visual stimuli|
|– Decreased responsiveness to food/odour|
|– Pacing/wanders aimlessly|
|– Snaps at air/licks air|
|– Licking – owners/household objects|
|– Increased appetite|
|Activity -apathy / depressed|
|– Decreased interest in food/treats|
|– Decreased exploration / activity|
|– Decreased interest in social interactions/play|
|– Decreased self-care|
|Sleep-Wake cycles /reversed day-night schedules|
|– Restless sleep / waking nights|
|– Increased daytime sleep|
|Learning and memory – house soiling|
|– Indoor elimination when previously trained|
|– Decrease/loss of signalling “need to go”|
|– Goes outdoors /then goes indoors again and eliminates|
|– Elimination in sleeping area|
|Learning and memory – work/tasks/commands|
|– Impaired working ability-decreased ability to perform task|
|– Decreased responsiveness to familiar commands|
|– Inability/slow to learn new tasks|
|Client Assessments Tool of Canine Patients for Cognitive Dysfunction (Rofina et al 2006)|
|Increased with diarrhoea||3|
|Increased without diarrhoea||4|
|Urinates and defecates indoors||4|
|Sleeps in day, restless at night||3|
|No aimless behaviour||1|
|Loss of Perception|
|Collides into furniture||2|
|Tries to pass thro’ narrow spaces||5|
|Tries to pass thro’wrong side of door||5|
|On new walks||2|
|On daily walks||4|
|No recognition of acquaintances||2|
|No recognition of owner after a break||4|
|No recognition of owner on a daily basis||5|
|Aggressive towards other pets/children||3|
|Aggressive towards the owner||4|
(Fast et al 2013,JVIM 27))
|Borderline cognitive dysfunction||11-15|
|Clinical cognitive dysfunction||15-41|
Many of the behavioural complaints of older pets are related to anxiety, including an increased prevalence of separation anxiety, phobias, excessive vocalisation, aggression and waking at nights. Not all such changes in the older dog are due to cognitive dysfunction . Other disease process which may cause or contribute to these signs must be excluded.(Table 3)
|Medical conditions which can cause behavioural problems|
|Neurological disease (brain neoplasia):||Changes in temperament , vocalisation , sleep wake changes , altered awareness, disorientation , confusion
|Partial seizures (temporal lobe epilepsy)||Repetitive/stereotypic behaviour behaviours, self-trauma, changes in temperament
|Feline hyperthyroidism||Irritability, aggression, decreased/increased activity, night waking|
|Lethargy, decreased response to stimuli, irritability/aggression|
|Altered appetite, house soiling, anxiety , decreased activity|
|Irritability/aggression, anxiety, lethargy, house soiling, altered appetite|
|Functional ovarian/testicular tumours||Male: aggression, roaming, marking, mounting objects
Female: nesting, possessive aggression
|Signs associated with organ affected:|
|Pain||Altered response to stimuli, decreased activity, restlessness, unsettled, vocalisation, house soiling, aggression/irritability, self-trauma, waking at night|
|Peripheral neuropathy||Self-mutilation, aggression/irritability, circling, hyperaesthesia|
|Gastrointestinal||Licking, polyphagia, pica, coprophagia, house soiling, unsettled sleep.|
|Urogenital||House soiling, waking at night|
|Dermatologic||Psychogenic alopecia (cats) acral lick granuloma, self-trauma (licking/chewing/biting/sucking)|
Because neurophsychological testing procedures of dogs and cats are now standardised therapeutic interventions can now also be evaluated and in some cases, approved, for use in clinical cases. Drugs, dietary changes and environmental enrichment and adjustment are the three mainstays of treatment.
Drugs: (See table 4)
|Drug Doses for Behaviour Therapy|
|Alprazolam||0.02 -0.1 mg/kg bid -qid||0.125-.025mg/cat oid – tid|
|Diazepam||0.5 – 2 mg oid – qid||0.2 -0.5mg/kg bid – tid|
|Oxazepam||0.2 – 1mg oid – bid||0.2 – 0.5 mg/kg oid – bid|
|Clonazepam||0.1 – 1.0 mg/kg bid – tid||0.02 – 0.2 mg/kg oid – bid|
|Lorazepam||0.025 – 0.2mg/kg oid – tid||0.025 – 0.05 mg/kg oid – bid|
|Melatonin||3-9 mg/dog||1.5 – 6 mg/cat|
|Diphenhydramine||2-4 mg /kg||1-4 mg/kg|
|Fluoxetine||1.0 – 2.0 mg/kg oid||0.5 – 1 mg/kg oid|
|Sertraline||1-5 mg/kg oid or 2.5 mg/kg bid||0.5 – 1.5 mg/kg oid|
|Buspirone||0.5 – 2.0 oid – tid||0.5 – 1 mg bid|
|Trazadone||2 – 5mg/kg as needed up to 8 – 10mgmg bid – tid||Not determined|
|Phenobarbital||2.5 – 5mg/kg bid||2.5 mg/kg bid|
|Gabapentin||10 – 30 mg /kg bid -tid||5 – 10mg/kg oid -tid|
|Potassium bromide||10 – 35 mg/kg daily or in divided doses||Not recommended|
|Selegiline||0.5 – 1 mg/kg oid in the am||0.5 – 1 mg/kg oid in am|
|Memantine||0.3 – 1 mg/kg oid||Not determined|
|Amantadine||1.25 – 4 mg/kg per os oid -bid||3mg/kg per os oid|
Selegiline is a selective irreversible monoamine oxidase B inhibitor (MAOB). The mechanism by which it causes its effect in dogs is not clear but three concurrent actions are proposed:
- increases 2-phenyl ethylamine (PEA) in the dog brain, a neuromodulater which enhances dopamine and catecholamine function and itself enhances congnitive function. Catecholamine enhancements may lead to enhance neuronal transmission. S
- contributes to decreasing the free radical load in the brain by scavenging free radicals and enhancing scavenging enzymes such as superoxide dismutase (SOD) and catalase.
- is neuroprotective effect on dopaminergic, noradrenergic and adrenergic neurons
Dose: 0.5 – 1 mg /kg oid in am. If there is not significant improvement in 30 days the dose can be adjusted upwards for another month. Toxicity can occur if used concurrently with other MOAIs.
Drugs for enhancing cerebral perfusion
Propentophylline (KarsivanÒ) is licensed for the treatment of dullness and lethargy in older dogs
Drugs enhancing the noradrenergic system:
Nicergoline : alpha 1 and alpha 2 adrenergic antagonist.
Adrafanil, modafinil: enhance noradrenergic system –improve alertness and help maintain normal sleep-wake cycle by increasing daytime exploration and activity. The noradrenergic system helps to maintain alertness, wakefulness, attention, memory and learning and also functions in neuroprotection. Treatment with these drugs causes improved learning but long term decreased memory – highlighting the need to test the full cognitive range when evaluating an intervention.
Anxiolytics and antidepressants:
Alterations in neurotransmission can lead to irritability, decreased responsiveness to stimuli, fear, and agitation. Antidepressants and anxiolytics may be considered in some older pets. These include clomipramine , amitriptyline, fluoxetine, and paroxetine benzodiazepines and buspirone.
Cholinergic function in the brain is important for memory and older dogs show a greater sensitivity to cholinergic disruption which impairs working memory. Clomipramine, paroxetine and amitryptiline are anticholinergic and should be used with care – drugs selected should also enhance and not reduce neuronal cholinergic activity if possible.
Dietary strategies involve supplementation with anti-oxidants and mitochondrial co-factors to improve anti-oxidant defences as well as reduce production and toxic effects of, and increase clearance of, oxygen free radicals. Vitamins E and C, beta-carotene, selenium, and other flavonoids and carotenoids from fruits and vegetables have antioxidant and anti-inflammatory properties in the treatment of cognitive dysfunction. B vitamins (thiamine, riboflavin, niacin b6 and B12)may also have antioxidant and neuroprotective effects as well as the ability to normalise neurotransmitter levels. Enhancement of mitochondrial function is achieved with the addition of L-carnitine and DL-alpha-lipoic acid.
The efficacy of Hills B/D has been evaluated over a trial period of 2 years using neurophsychological testing well as in clinical trials and was found to improve performance on a number of cognitive tasks beginning as early as 2-8 weeks after onset of the diet. In a 60 day double blinded clinical trial of 142 dogs there was a significantly greater improvement in cognitive function in the treated group than in the control group.
Traditional ketogenic diets are high in fat low in protein and very low in carbohydrates, this is unsuitable for old dogs due to protein catabolism and muscle wasting which normally occurs in ageing. Dietary medium chain triglyceride (MCT) supplementation can increase blood ketone body levels without restricting dietary proteins and carbohydrates. This increased supply of an alternative energy source can improve cognitive performance. A diet containing MCT (Purina One Vibrant Maturity 7+ for dogs)has been shown to improve cognitive function.
Instead of only focusing on the treatment of clinical signs more effort should be made to utilise the many products containing antioxidant and neuroprotective substances to slow the progression of the disease by starting treatment at an earlier age, even before owners detect cognistive impairment as laboratory test have shown impairment starts insidiously from about 7 years of age.
Dogs without environmental enrichment show a more rapid decline in cognitive function. The dogs in the groups with dietary supplementation (Hills B/D) or environmental enrichment did better than those control animals without dietary or environmental improvements. The greatest effect was seen with combined dietary supplementation and environmental enrichment.
Practical tips: Food puzzle toys, interactive toys, play and exercise and training, night light as vision deteriorates, help maintain temporal orientation with odours (scented candles), tactile (flooring) and auditory cues to help. Pherormone therapy as an anxiolytic (FeliwayÒ). Keep up a predictable routine to reduce anxiety, and keep the dog active during the day so that it sleeps at night. Training , play exercise and novelty toys.
Cognitive dysfunction in cats is not as clearly researched as in dogs. Old age in cats is accompanied by altered behaviour such as wandering, vocalisation and night time activity , which are not attribuible to medical problems. These changes can start from about 10 years of age with a significant increase in older cats. Cats are more likely to present with excessive vocalisation and night time activity. Several supplements for senior cats are available in Europe : Cholodin-Fel (MVP Labs) , Senilife (CEVA Animal Health), Activaite (VetPlus).