Changes in the aging canine brain have also been described on magnetic resonance images.30,31 There is progressive cortical atrophy and ventricular enlargement as dogs age. The brain blood volume does not change with
age, and a nonsignificant trend toward increasing blood-brain barrier permeability exists.30 A detailed study revealed that the frontal lobe of the canine brain atrophies earlier than the rest of the brain.31
What is the age range for the onset of these changes in dogs? How do they manifest clinically?
Histopathologic changes are seen as early as 2 to 3 years of age (e.g. lipofuscin accumulation) and accumulate throughout life.29 Frontal lobe atrophy was detected in beagles aged 8 years and older, perhaps correlating with the age at which β-amyloid
deposits appear. Ventricular volume (as an indicator of cerebral atrophy) started to increase at 10 to 11 years of age. Whole
brain atrophy was not evident until 12 years of age.31
The clinical significance of these changes in pet dogs is unclear. The extent of β-amyloid protein deposition has been correlated
with the severity of deficits in cognition and memory tasks in experimental dogs.32,33 In addition, MRI studies have shown that frontal lobe atrophy correlates to reduced performance of dogs in memory tests.30,31 Determining the significance of the presence of Lafora's bodies and lipofuscin is problematic (because these changes can
also occur with normal aging), as diseases with excessive numbers of Lafora's bodies and a storage disorder (ceroid lipofuscinosis)
that are associated with neurodegenerative changes have been described.3 In general, however, such findings are not thought to cause neurologic deficits.
What types of age-related changes occur in the feline brain?
Little information is available on the changes present in the aging feline brain. The published data report on a limited number
of animals.33,34 Data presented at the 2004 American College of Veterinary Internal Medicine Forum described the accumulation of β-amyloid
peptide in the brains of cats.35 The location of the plaques was similar to that in dogs and people, but the composition of the plaques differed in terms
of the peptide fragments present. Unlike in dogs, there is hippocampal accumulation of hyperphosphorylated tau protein, the
component of neurofibrillary tangles, in the brains of aged cats.
What is the age range for the onset of these changes in cats? How do they manifest clinically?
Longitudinal neuropathologic studies have not been performed in cats, making it difficult to know when the changes first appear.
One of the published studies looked at cats that were 18 years or older.34 The clinical significance of these findings is unknown.
Can anything be done to help prevent, slow, or reverse these changes in dogs and cats?
Careful studies have been completed on the effect of dietary antioxidants on the cognitive changes associated with aging in
dogs.36 One placebo-controlled study was done on experimental colonies of beagles. Their diet was supplemented with antioxidants,
mitochondrial cofactors, and a variety of flavonoids and carotenoids designed to protect against oxidative damage and to support
mitochondrial function. The results showed that six months of dietary modification significantly reduced age-associated cognitive
decline. These studies did not include histologic evaluation of the brain, so conclusions about pathologic changes cannot
be made. A blinded clinical trial in dogs with age-related cognitive decline that compared the effect of a similarly fortified
diet with a control diet showed that dogs receiving the fortified diet had significant improvements in compulsive behavior,
agility, and recognition of owners and other dogs as scored by the owner.37