Nutritional management of canine brain aging
Improved nutrition and medical care have prolonged life spans in both people and their pets. Current estimates suggest that there are approximately 20 to 30 million senior and geriatric dogs over the age of 7 years in the North America.
However, longer life may lead to an increased prevalence of age-related behavioral and cognitive problems.
Canine cognitive dysfunction syndrome (CDS) is the name proposed to describe the behavioral changes associated with brain aging in senior dogs. In examining the cases referred to veterinary behaviorists, the most common complaints of owners of senior dogs included separation anxiety, aggression to people, anxiety and phobias, housesoiling, night waking and vocalization. However, these cases do not accurately reflect the magnitude of the problem at the general practice level.
For example, using an owner-based observational questionnaire, 28 percent of the otherwise healthy dogs between the ages of 11 and 12, and 68 percent between the ages of 15 to 16 had signs of CDS in at least one of the following categories: disorientation, housesoiling, social interactions, sleep-wake cycles or activity levels.
Further, CDS may be progressive. Many aged dogs with impairments in one behavioral category were found to have impairments in two or more categories within 12 to 18 months.
The aged canine brain exhibits several key features that can also be observed in the aging human brain.
Aged canine brains display a number of morphological changes similar to those observed in aged human brains, including cortical atrophy and ventricular widening, myelin degeneration in the white matter, accumulation of degraded proteins, DNA damage and reduction of endogenous antioxidants.
The aged canine brain also accumulates proteins within and around neurons that may be toxic. Accumulation of diffuse proteinaceous plaques has received the most attention in aged dogs because it is thought to play a causative role in development of human Alzheimer's disease.
Plaques contain a number of proteins, but the primary constituent is the β-amyloid peptide (Aβ), which has identical amino acid sequences in both people and dogs.
The extent of Aβ deposition in the canine brain is linked to the severity of cognitive deficits and behavioral changes.
A mechanism that may contribute to neuron dysfunction and progressive accumulation of neuropathologic lesions in aged brains is oxidative damage due to reactive oxygen species, which are formed as by-products of cellular metabolism.
Aerobic metabolism in mitochondria has been implicated in the production of the majority of reactive oxygen species.
As mitochondrian age or become dysfunctional from disease or stress, more reactive oxygen species form, which may then undergo further uncontrolled reactions within the cell. Brain aging is a cumulative response to these alterations and the associated neuropathology accounts for age-associated cognitive and behavioral changes.
The brain may be especially vulnerable to cumulative oxidative damage and aging due to its high metabolic rate (i.e., high demand for oxygen) and limited antioxidant defense and repair capabilities. The aging process also appears to be accompanied by a decreased ability to fight the effects of oxidative stress and decreased mitochondrial function, resulting in greater oxidative damage.
The advanced learning ability of dogs is well known as evidenced by their use as assistance companions (e.g. guide dogs) and working animals (e.g. military, search and rescue dogs).
Learning and memory can be tested systematically in dogs using tasks developed for use in nonhuman primates.
In parallel with human and primate studies, tasks are selected that are sensitive to the function of specific brain cortical circuits or regions. All testing is conducted using food rewards, which sufficiently motivate dogs to learn each task.