There is no cure for canine cognitive dysfunction, but there are medical aids to help mask the symptoms attributed to the disease as it progresses. Therapies are a major form of symptom masking, such as exercise increase, new toys, and learning new commands have shown increases in memory. Changing the dog's diet is also a helpful tool in improving memory and cell membrane health. Medication is also one of the most effective ways to mask the symptoms of CCD. Anipryl (selegiline) is the only drug that has been approved for use on dogs with canine cognitive dysfunction. Anipryl is a drug that is used to treat humans with Parkinson's disease, and has shown drastic improvement in the quality of life in dogs living with CCD.

In order for dogs to cope with CCD with as little frustration as possible, it is important to make the transition into the progression of the disease easy and stress free. The environment in which the dog lives is prevalent in the coping process. To keep the environment familiar to the dog, consider eliminating clutter around the house to prevent obstacles for the dog, keep commands short as to avoid confusion, immerse the dog in short, friendly play sessions, and develop a feeding and watering schedule that sticks to a routine. Avoid changing decorations or rearranging furniture in the house, as this will avoid confusion and problems with moving around. When these precautions are taken, the dog will have a higher chance of living longer with as little effects of CCD as possible.

CTD is difficult to treat because the actual transporter responsible for transporting creatine to the brain and muscles is defective. Studies in which oral creatine monohydrate supplements were given to patients with CTD found that patients did not respond to treatment. However, similar studies conducted in which patients that had GAMT or AGAT deficiency were given oral creatine monohydrate supplements found that patient’s clinical symptoms improved. Patients with CTD are unresponsive to oral creatine monohydrate supplements because regardless of the amount of creatine they ingest, the creatine transporter is still defective, and therefore creatine is incapable of being transported across the BBB. Given the major role that the BBB has in the transport of creatine to the brain and unresponsiveness of oral creatine monohydrate supplements in CTD patients, future research will focus on working with the BBB to deliver creatine supplements. However, given the limited number of patients that have been identified with CTD, future treatment strategies must be more effective and efficient when recognizing individuals with CTD.

There is no specific treatment but triggering anesthetics are avoided and relatives are screened for "RYR1" mutations as these may make them susceptible to MH.

Central core disease (CCD), also known as central core myopathy, is an autosomal dominant congenital myopathy (inborn muscle disorder). It was first described by Shy and Magee in 1956. It is characterized by the appearance of the myofibril under the microscope.

Creatine transporter defect (CTD) is an inborn error of creatine metabolism in which creatine is not properly transported to the brain and muscles due to defective creatine transporters. CTD is an X-linked disorder caused by mutations in the SLC6A8 gene. The SLC6A8 gene is located on the short arm of the sex chromosome, Xq28. Hemizygous males with CTD express speech and behavior abnormalities, intellectual disabilities, development delay, seizures, and autistic behavior. Heterozygous females with CTD generally express fewer, less severe symptoms. CTD is one of three different types of cerebral creatine deficiency (CCD). The other two types of CCD are guanidinoacetate methyltransferase (GAMT) deficiency and deficiency. Clinical presentation of CTD is similar to that of GAMT and AGAT deficiency. CTD was first identified in 2001 with the presence of a hemizygous nonsense mutation in the SLC6A8 gene in a male patient.

Observations leading to the characterization of the SLC26 family were based on research on rare human diseases. Three rare recessive diseases in humans have been shown to be caused by genes of this family. Diastrophic dysplasia, congenital chloride diarrhea, and Pendred syndrome are caused by the highly related genes SLC26A2 (first called DTDST), SLC26A3 (first called CLD or DRA), and SLC26A4 (first called PDS), respectively. Two of these diseases, diastrophic dysplasia and congenital chloride diarrhea, are Finnish heritage diseases.

Available treatments address the symptoms of CCD, not the underlying defect. Early diagnosis and aggressive salt replacement therapy result in normal growth and development, and generally good outcomes. Replacement of NaCl and KCl has been shown to be effective in children.

A potential treatment is butyrate.

Cerebral creatine deficiencies (CCD's) are a small group of disorders mainly concerned with creatine biosynthesis and utilization in the brain at the blood-brain interface. The most common CCD is:

- creatine transporter defect (CTD), an X-linked condition caused by mutations in the "SLC6A8" gene.

The two other forms of CCD are creatine "enzymatic" defects (CED's) in creatine biosynthesis, i.e. the enzyme deficiencies:

- , and

- guanidinoacetate methyltransferase deficiency.

Several studies have reported that life expectancy appears to be normal for people with CCD.

Around 5 years of age, surgical correction may be necessary to prevent any worsening of the deformity. If the mother has dysplasia, caesarian delivery may be necessary. Craniofacial surgery may be necessary to correct skull defects. Coxa vara is treated by corrective femoral osteotomies. If there is brachial plexus irritation with pain and numbness, excision of the clavicular fragments can be performed to decompress it. In case of open fontanelle, appropriate headgear may be advised by the orthopedist for protection from injury.