“The similarity of CCD to Alzheimer’s in humans is therefore not a coincidence, AS THE MANNER IN WHICH THE BRAIN CHANGES IN THE TWO CONDITIONS IS FOUND TO BE VERY SIMILAR.”
in the house, yet have nothing to do with CCD. Hyperadrenocorticism (HAC, or Cushing’s disease) is a common cause of dysthymia-like symptoms which are unrelated to the progression of CCD. Rather, it is a common endocrine syndrome that happens to affect middle-aged and older dogs. HAC is generally caused by tumors of either the pituitary or adrenal glands 3 and is sometimes the result of long-term steroid therapy. These examples show that when standard tests reveal no physiologi- cal cause for the CCD symptoms, it is time to consider CCD as the root cause. PHYSIOLOGICAL CAUSES OF CCD The underlying cause(s) of CCD are not fully understood, but its onset is always associated with the develop- ment of accumulations of sticky pro- teins called “beta-amyloid plaques” around neurons, and the breakdown of the neurons themselves, resulting in so-called neurofibrillary tangles. These plaques and tangles are seen to inhibit the normal functioning of the inter-cellular communication re- quired by the nervous system. In the body, nerve cells fire nerve impulses to release neurotransmitters, which are just chemicals that carry signals to other cells (including other nerve cells). These relay their message by traveling between cells and attach- ing to receptors on target cells. Some of the most familiar transmitters are serotonin, dopamine, acetylcholine, endorphins, and epinephrine. These are actually just a few of more than one hundred that have been identified and associated with control of one or more specific functions. Each neurotransmitter attaches to a unique receptor—for example,
dopamine molecules attach to dopa- mine receptors. Upon attachment, they trigger a specific action in the target cells. There are (1) excitatory neurotransmitters which encour- age a target cell to take action, (2) inhibitory neurotransmitters which decrease the chances of the target cell taking action, and (3) modula- tory ones which signal many neurons at the same time, as well as commu- nicate with other neurotransmit- ters. After completing their function, neurotransmitters are either broken down or recycled by the body. The brain, in particular, uses neu- rotransmitters to regulate many necessary functions, including heart rate, breathing, sleep cycles, appetite, digestion, mood, concentration, and muscle movement. One can therefore see that the interference in neural communication caused by plaques and tangles can change the normal functions into the ones we likely as- sociate with CCD. As a simple example, Serotonin has a profound affect over emotions and regulates mood, enhances a positive feeling, and inhibits aggressive re- sponse, while Dopamine helps to fo- cus attention and promotes feelings of satisfaction. A lack of these two neurotransmitters can cause irrita- bility, limited impulse control, over reactivity, including hyper-aggres- sion and anxiety, and greater sensi- tivity to pain. The similarity of CCD to Alzheimer’s in humans is therefore not a coinci- dence, as the manner in which the brain changes in the two conditions is found to be very similar. Both humans with Alzheimer’s and dogs with CCD get the beta-amyloid plaques and neurofibrillary tangles which block the normal communication between
neurons by the neurotransmitters. 4 In both human and canine brains, be- ta-amyloid plaques are commonly de- tected in extracellular space as senile plaques and also around the blood vessels. 5 While the neurotransmitter chemicals are themselves identical in dogs and humans, their detailed impact on behavior (such as the way emotions are processed) may differ between the species simply because of differences in the geometry of their brains. Nevertheless, the result is that dogs exhibit impairment in many men- tal processes that directly paral- lel human symptoms, such as dis- orientation, memory loss, changes in behavior, and changes in mood, which can include hyper-aggression, and these are all tied to degrada- tion in the performance of their CCD is currently considered irrevers- ible—there is no cure for CCD. How- ever, some of the four separate cogni- tive manifestations of CCD may be preventable, and some symptoms can be minimized. common neurotransmitters. TREATMENT OF CCD: Thedrug that isprimarilyusedtotreat CCD by improving brain functions is selegiline(Anipryl). It isamonoamine oxidase inhibitor (MAOI) thought to improve brain chemistry by reduc- ing the breakdown of dopamine and other neurotransmitters. Other drug treatments include Nicer- goline, which is prescribed in the UK, and Propentofylline, used in some European countries and in Australia. The former enhances blood flow to the brain and is thought to enhance the transmissions of neurons. The latter drug is thought to increase blood flow by making the red blood
32 • T op N otch T oys , N ovember 2021
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