Canavan Disease

Updated October 11, 2020

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What is Canavan Disease?

Canavan disease damages the ability of nerve cells in the brain to send and receive messages. 1

It is a rare inherited disorder that is part of an overarching group of genetic conditions known as leukodystrophies. 2

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All leukodystrophies affect white matter in the brain, or areas of the brain that appear white on brain imaging tests like a computed tomography (CT) scan. White matter is actually the myelin sheath, which is a material made of proteins and fat that surrounds and protects nerve cells.

The myelin sheath allows electrical impulses to travel quickly and efficiently throughout the brain – these electrical impulses are how nerve cells in our brain coordinate behavior, sensation, thoughts, and emotion. 3

When damage to the myelin sheath occurs, it can slow down or block electrical impulses between the brain and the rest of the body. 4

Canavan disease was first described in 1931 by Dr. Myrtelle Canavan, one of the first female neuropathologists. 5 Dr. Canavan described the degeneration of white matter as well as an enlarged head in a child who was thought to have a different disease.

The majority of leukodystrophies, including Canavan disease, appears in infancy or in early childhood. Children may appear initially healthy, but symptoms gradually appear and worsen over time, resulting in these individuals being unable to hear, see, speak, or move. 6

Canavan disease is a genetic disease, and is caused by a mutation in a gene called ASPA, which provides the body with instructions for making an enzyme called aspartoacylase. 7

Aspartoacylase is responsible for breaking down the concentrated brain chemical known as N-acetyl-aspartate (NAA). NAA was thought to play a role in developing and maintaining white matter in the brain, but recent studies have found that it may instead play a role in transporting water molecules out of the neurons. 8

Without proper aspartoacylase function, NAA accumulates in the brain and causes the symptoms associated with Canavan disease.

There are 2 types of Canavan disease: infantile and juvenile. The infantile is the most common and the most severe form of the disorder. 9 Infants with Canavan disease will appear normal for the first months of life, but between 3 to 5 months symptoms typically develop.

These infants typically do not develop motor skills like rolling over, controlling their head, and sitting. These infants tend to have hypotonia, or a lower muscle tone, a larger head, or macrocephaly, and some behavioral symptoms like irritability or sleep disturbances. 10

A juvenile form of Canavan disease is less common and causes milder symptoms. In this type of Canavan disease, there is usually a mild delay in speech and language development, but these delays are typically so mild that they are not diagnosed as being caused by Canavan disease. 11

Life expectancy for people with Canavan disease varies. Those with the neonatal/infantile form usually only live until childhood, although there are some individuals who live into adolescence. Individuals with the juvenile form do not typically experience any changes in life expectancy. 12

There are no cures or standard treatments for Canavan disease, but medications, speech therapy, and physical therapy may help with easing some of the symptoms. 13

Causes and the Genetic Pattern of Inheritance for Canavan Disease

Canavan disease is an inherited condition that occurs when variations, or changes, of the ASPA gene pass from one generation to the next. 14 

Our bodies are made of millions of cells, and in each of our cells we have 23 pairs of chromosomes, or 46 total. In each pair, one member is from our mother and the other from our father. Chromosomes are tightly wound DNA, which holds all of our genetic material. DNA can be divided into genes, or portions of DNA that provide the body with instructions on how to make certain proteins that help us to develop, function, and reproduce.

Since our chromosomes come in pairs, our genes come in pairs as well, which means that we have 2 copies of each of our genes.

Canavan disease is inherited in an autosomal recessive pattern. This means both copies of the ASPA gene have a pathogenic variant, or a variation in the ASPA gene that does not allow it to function properly. 15

Inheriting two copies of the ASPA gene with a pathogenic variant  may occur if each parent carries one copy of the changed gene – these parents would not show signs or symptoms of the disease, but they are at risk of passing the disease down to their children. 16

ASPA is needed to provide the body with instructions for producing the enzyme aspartoacylase, which degrades NAA. If ASPA is non-functional and the body does not produce sufficient amounts of aspartoacylase, NAA accumulates in the brain and causes the symptoms associated with Canavan disease. 17

Who Is Impacted by Canavan Disease?

Canavan disease affects all ethnic groups, but it is more frequent in individuals with Ashkenazi Jewish descent.

In the general population, the carrier rate for Canavan disease is unknown, but it is estimated to be about 1/300 – this is markedly different when compared to the carrier rate in the Ashkenazi Jewish population, where the carrier rate is about 1/40. 18

A carrier will not have signs and symptoms of Canavan disease because they have one functional copy of the ASPA gene, but their other copy of the ASPA gene has a pathogenic variant that may be passed down to their children.

If both parents are carriers, each of their children has a 25% chance of inheriting both of their parents’ changed gene, a 50% chance of being a carrier where they inherit one functional ASPA gene and one non-functional copy, and a 25% chance of being neither a carrier nor impacted by Canavan disease if they inherit both functional copies from their parents. 19

Canavan disease occurs in people of all ethnic backgrounds but it is most common in individuals of Ashkenazi Jewish heritage, impacting 1 in 6,400 to 13,500 people in the Ashkenazi Jewish population. 20

Certain genetic disorders are more commonly seen in different ethnic groups because of a phenomenon known as the Founder Effect, or a lack of genetic diversity that occurs when an ethnic group is descended from a small number of ancestors. Hundreds of years ago, variations occurred in the genes of some individuals within an ethnic group.

These individuals were then considered carriers where they did not have any of the genetic disorders associated with the newly changed genes, but their descendants were at a higher risk of developing those genetic disorders – this explains why now there are certain ethnic groups that experience higher rates of some genetic disorders. 21

Signs and Symptoms of Canavan Disease

The signs and symptoms of Canavan disease depends on whether an individual has the infantile or juvenile type.

The infantile type of Canavan disease is the most common and severe form. Infants with this form of Canavan disease appear normal for the first few months of life, but by age 3 to 5 months, developmental problems are typically noticeable.

Most affected infants do not develop motor skills such as turning over, controlling head movement, and sitting without support – this is mostly due to most infants with Canavan disease having hypotonia, or a low muscle tone. Hypotonia also causes these infants to have difficulty feeding and swallowing. Affected infants also have macrocephaly, or an unusually large head size, and behavioral problems like irritability and sleep disturbances. 22

As these affected infants age, they begin to experience psychomotor regression which means that these infants are no longer able to perform developmental milestones that they had previously achieved. Intellectual disability develops, and hypotonia typically transitions into spasticity, or involuntary muscle spasms that cause slow and stiff movements of the arms and legs.

Eventually, these infants experience rigidity or paralysis in all of their extremities as well as seizures and the degradation of nerve cells in the eye, which may lead to blindness. 23

Individuals with the juvenile form of Canavan disease have far milder symptoms that are not typically life-threatening and may produce only minor developmental delays, if any at all. The juvenile form of Canavan disease is uncommon, and these individuals typically have delayed speech development and motor skills starting in childhood.

These delays may be so mild they are never recognized as being caused by Canavan disease. These individuals also do not experience any type of regression, vision loss, or seizures, and they also typically do not have any of the physical features seen in the infantile form, like macrocephaly or hypotonia. 24

The life expectancy for individuals with Canavan disease varies and depends on the form of Canavan disease. Children born with the infantile form of Canavan disease typically only live into childhood, but some do survive into adolescence. 25

Individuals with the juvenile form of Canavan disease do not experience any change to life expectancy. 26

Diagnosis of Canavan Disease

Receiving a diagnosis of Canavan disease typically requires a variety of tests, including genetic testing.

The ASPA gene provides the body with instructions for producing an enzyme called aspartoacylase, which degrades the protein NAA in the brain. Children born with Canavan disease do not produce sufficient aspartoacylase, causing them to accumulate high levels of NAA over time. 27

One of the first methods of diagnosing Canavan disease is a urinalysis, which evaluates the presence or absence of certain molecules in the urine; for individuals with Canavan disease, their urine will have higher than normal NAA. Besides urine, NAA levels can also be detected in the blood or cerebrospinal fluid.

Alongside a urinalysis, individuals with Canavan disease may undergo tests that evaluate aspartoacylase enzyme activity – this can be tested via skin cells or blood. 28

These two tests are preliminary diagnostic measures that are typically completed alongside a clinical examination. In a clinical evaluation, a trained physician reviews an individual’s physical symptoms to see if they may align to a Canavan disease diagnosis.

A psychologist may also participate in the clinical examination to evaluate the individual’s achieved verbal milestones, since Canavan disease is associated with psychomotor regression. Brain imaging may also be ordered to assess white matter levels. 29

While other tests are being administered, a DNA test may be completed as well to see if there are pathogenic variants present in an individual’s ASPA genes. A DNA test is the most accurate way to test for Canavan disease. 30

Testing for Canavan disease on a Pregnancy or Before a Pregnancy is Achieved

Testing for Canavan disease during pregnancy versus before pregnancy requires two different types of testing. During pregnancy, the fetus can be tested using amniocentesis or chorionic villus sampling (CVS). 31

Before pregnancy, both reproductive partners may be tested to see if they are carriers for Canavan disease via DNA testing.

Amniocentesis and CVS are both diagnostic procedures that can be done during pregnancy to evaluate the fetus for genetic abnormalities. Amniocentesis is completed between the 15th and 20th week of pregnancy and entails a long, thin needle being inserted through the abdomen to collect a small sample of amniotic fluid, which is the fluid that surrounds the fetus in utero.

Amniotic fluid holds skin cells from the fetus that have naturally sloughed off as the fetus moves and develops, and the skin cells hold DNA that can be used for genetic testing. 32 The amniotic fluid can also be evaluated for NAA levels, which can suggest Canavan disease if elevated. 33

CVS is completed between the 11th and 14th week of pregnancy and entails a long, thin needle being inserted through either the abdomen or the cervix to extract a tiny sample of the placenta, which holds the fetus during pregnancy. The placenta typically has the same DNA as the fetus, although there is a less than 1% chance of there being confined placental mosaicism, meaning that the placenta’s genetic information does not match the fetus’ genetic information 34.

For both CVS and amniocentesis, there is about a 1 in 500 risk for miscarriage, infection, or bleeding, but both procedures assign a diagnosis to the fetus that can be used to make decisions about continuing the pregnancy and the actual birth. 35

It is important to note that parents pursuing prenatal testing for Canavan disease must have a known pathogenic mutation that the fetus can undergo specific genetic testing for. Additionally, while it's beneficial in determining a Canavan disease diagnosis early, it doesn't help with the prognosis.

DNA testing can determine whether or not you have Canavan disease, but it does not predict life expectancy or severity of symptoms. 36

Carrier Screening for Canavan Disease

If both parents are carriers of a pathogenic variant for Canavan disease, each child has a 25% chance of being born with Canavan disease. 37

Individuals may choose to assess their risk of passing down Canavan disease to future pregnancies by assessing if they are carriers of Canavan disease. 38 Genetic testing can determine if a pathogenic variant is present before parents decide to go forward with starting a family.

Carrier screening is recommended for all pregnant women or women who are thinking about becoming pregnant. In the general population, carrier screening looks at recessive genetic disorders that are common across all ethnicities, like cystic fibrosis.

However, individuals of certain ethnicities, like Ashkenazi Jewish, are impacted by the Founder Effect, so they are more likely than the general population to be carriers for a number of genetic disorders. Because of this, individuals of certain ethnic backgrounds may consider targeted carrier screening which screens for genetic disorders based on ethnicity. Canavan disease is included on targeted carrier screenings for individuals of Ashkenazi Jewish descent. 39

Carrier screening can be ordered by a genetic counselor, who can also provide guidance and education on a wide variety of genetic issues, including Canavan disease, before conception or during pregnancy.

If both parents are found to be carriers for Canavan disease or a parent is affected by juvenile Canavan disease, they may choose in-vitro fertilization (IVF) and pre-implantation genetic diagnosis (PGD). IVF is a method of assisted reproductive technology where a woman’s eggs and a man’s sperm are combined to create embryos in a lab that can then undergo PGD, or genetic testing for genetic disorders like Canavan disease, prior to being implanted into the carrier of the pregnancy.

With this method, only embryos that do not have genetic abnormalities are attempted to be implanted. 40

Treatments and Care Options for Canavan Disease

There is no cure for Canavan disease, and there is no established treatment protocol – treatment is largely supportive and aims to ease symptoms. 41

Supportive care is critical to ease the symptoms of the disease. This means supplying patients with adequate nutritional needs and hydration as their feeding abilities regress, protecting the airway, and treating any infectious diseases as soon as possible. 42

Physical therapy can also help to reduce the severity of the spasticity symptoms and improve motor abilities as well as seating posture. Seizures are treated with anti-epileptic drugs and speech therapy may assist with communication skills. 43

There are currently investigations into drug therapies for Canavan disease, but there is no established standard of treatment. Gene therapy for Canavan disease is also currently under investigation -- gene therapy involves delivering a functional copy of the APSA gene that replaces the non-functional copy.

Researchers have proven that they are able to replace the ASPA gene, but they are still investigating long-term effects of this therapy as well as whether it reverses damage that has been done due to NAA accumulation. 44

The best medical advice and treatment is provided by doctors who have experience with Canavan disease. A genetic counselor or your primary care physician can help connect you with experienced specialists.

Complications Associated with Canavan Disease

There are a number of complications associated with Canavan disease that are often fatal. 45

Canavan disease leads to myelin sheath degradation, which initially appears as developmental delay but quickly transitions to psychomotor regression, meaning that these individuals lose any developmental milestones that they had previously achieved. Infants with Canavan disease are hypotonic, meaning that they have a low muscle tone, and at the time that psychomotor regression begins this hypotonia transitions to uncontrolled rigid extensions and rotations of the extremities.

Another complication of psychomotor regression is profound intellectual disability and potentially seizures. 46

As Canavan disease progresses, individuals may experience degradation of nerves associated with the eye, which leads to nystagmus, or rapid, involuntary eye movements, and blindness. In some cases, the nerves within the ear may also degrade which can lead to hearing loss, but this is rare. 47 

The Prognosis of Canavan Disease

The prognosis for people with Canavan disease is poor for those with the more severe infantile form of the disease.

Individuals with the infantile form of Canavan disease and severe symptoms typically do not survive past 18 months, and most individuals with the infantile form do not survive past the age of 10. 48 However, a few cases have survived into adolescence and early adulthood.1 Life expectancy largely depends on the clinical course of the disease and the level of treatment, and both of these vary from person to person.

Individuals with the juvenile type of Canavan disease do not typically experience a shortened life span. 49

What to do Next: Living with Canavan Disease

There is currently no cure for Canavan disease, but various treatment methods can help to ease some symptoms.

A crucial part of a treatment plan for individuals with Canavan disease may be to connect with families or individuals who also experience Canavan disease in order to receive support. Meeting with a genetic counselor can help connect you to local resources.

The following resources can provide more information on Canavan disease:

National Organization for Rare Disorders: This provides educational resources about rare diseases like Canavan disease.

The Canavan Disease Patient Insights Network (PIN): This is a network to understand and share the health experiences of people with Canavan Disease. Privacy is protected, so participants can share de-identified data if they choose. Participants can also choose to receive notice of clinical trial recruitment and the latest research news.

Canavan Foundation, Inc.: This is a patient support organization for individuals and families who have experience with Canavan disease who are interested in support groups, educational resources, and community outreach.

Canavan Disease Research: This is a patient support organization for individuals and families with Canavan disease who are interested in participating in research.

Referenced Sources

  1. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  2. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  3. Bunge, R.P. (1968). Glial cells and the central myelin sheath. Physiological News, 48(1): 197-251.
  4. Bunge, R.P. (1968). Glial cells and the central myelin sheath. Physiological News, 48(1): 197-251.
  5. CANAVAN MM. SCHILDER'S ENCEPHALITIS PERIAXIALIS DIFFUSA: REPORT OF A CASE IN A CHILD AGED SIXTEEN AND ONE-HALF MONTHS. Arch NeurPsych. 1931;25(2):299–308.
  6. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  7. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  8. Baslow, M.H. (2003). N-Acetylaspartate in the Vertebrate Brain: Metabolism and Function. Neurochem Res 28, 941–953.
  9. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  10. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  11. Jauhari, P., Saini, L., Chakrabarty, B., Kumar, A., & Gulati, S. (2018). Juvenile Canavan disease: a leukodystrophy without white matter changes. Journal of Neuropediatrics, 49(6):420-421.
  12. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  13. Gordon, N. (2001). Canavan disease: A review of recent developments. European Journal of Paediatric Neurology, 5(2):65-69.
  14. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  15. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  16. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  17. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  18. Michals K, Matalon R. Canavan disease. In: Raymond GV, Eichler F, Fatemi A, Naidu S, eds. Leukodystrophies. London: Mac Keith Press; 2011:156-69
  19. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  20. Michals K, Matalon R. Canavan disease. In: Raymond GV, Eichler F, Fatemi A, Naidu S, eds. Leukodystrophies. London: Mac Keith Press; 2011:156-69
  21. Slatkin, M. (2004). A population-genetic test of founder effects and implications for Ashkenazi Jewish diseases. AJHG, 75(2):282-293.
  22. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  23. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  24. Jauhari, P., Saini, L., Chakrabarty, B., Kumar, A., & Gulati, S. (2018). Juvenile Canavan disease: a leukodystrophy without white matter changes. Journal of Neuropediatrics, 49(6):420-421.
  25. Kaul, R., Gao, G. P., Aloya, M., Balamurugan, K., Petrosky, A., Michals, K., & Matalon, R. (1994). Canavan disease: mutations among Jewish and non-Jewish patients. American journal of human genetics, 55(1), 34–41.
  26. Jauhari, P., Saini, L., Chakrabarty, B., Kumar, A., & Gulati, S. (2018). Juvenile Canavan disease: a leukodystrophy without white matter changes. Journal of Neuropediatrics, 49(6):420-421.
  27. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  28. Matalon, R. (2009). Canavan disease: diagnosis and molecular analysis. Genetic Testing, 1(1).
  29. Matalon, R. (2009). Canavan disease: diagnosis and molecular analysis. Genetic Testing, 1(1).
  30. Matalon, R. (2009). Canavan disease: diagnosis and molecular analysis. Genetic Testing, 1(1).
  31. Matalon, R., & Matalon, K. M. (2002). Canavan disease prenatal diagnosis and genetic counseling. Obstetrics and gynecology clinics of North America, 29(2), 297–304.
  32. Whittle, M.J. (1998). Randomised trial to assess safety and fetal outcome of early and midtrimester amniocentesis. The Lancet, 351(9098):242-247.
  33. Matalon, R., & Matalon, K. M. (2002). Canavan disease prenatal diagnosis and genetic counseling. Obstetrics and gynecology clinics of North America, 29(2), 297–304.
  34. Toutain, J., Goutte-Gattat, D., Horovitz, J., & Saura, R. (2018). Confined placental mosaicism revisited: Impact on pregnancy characteristics and outcome. PloS one, 13(4): e0195905.
  35. Mujezinovic, F. & Alfirevic, Z. (2007). Procedure-Related Complications of Amniocentesis and Chorionic Villous Sampling. Obstetrics & Gynecology,110(3): 687-694
  36. Matalon, R., & Matalon, K. M. (2002). Canavan disease prenatal diagnosis and genetic counseling. Obstetrics and gynecology clinics of North America, 29(2), 297–304.
  37. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  38. Matalon, R., & Matalon, K. M. (2002). Canavan disease prenatal diagnosis and genetic counseling. Obstetrics and gynecology clinics of North America, 29(2), 297–304.
  39. Grody, W., Cutting, G., Klinger, K. et al. (2001). Laboratory standards and guidelines for population-based cystic fibrosis carrier screening. Genet Med 3, 149–154.
  40. Danilo Cimadomo, Laura Rienzi, Antonio Capalbo, Carmen Rubio, Federica Innocenti, Carmen María García-Pascual, Filippo Maria Ubaldi, Alan Handyside. (2020) The dawn of the future: 30 years from the first biopsy of a human embryo. The detailed history of an ongoing revolution. Human Reproduction Update 26(4): 453-473.
  41. Zelnik, N., Luder, A.S., Elpeleg, O.N., Gross-Tsur, V., Amir, N., Hemli, J.A., Fattal, A., & Harel, S. (1993). Protracted Clinical Course for Patientsd with Canavan Disease. Developmental Medicine and Child Neurology, 35(4).
  42. Zelnik, N., Luder, A.S., Elpeleg, O.N., Gross-Tsur, V., Amir, N., Hemli, J.A., Fattal, A., & Harel, S. (1993). Protracted Clinical Course for Patientsd with Canavan Disease. Developmental Medicine and Child Neurology, 35(4).
  43. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  44. Leone, P., Shera, D., McPhee, S. W., Francis, J. S., Kolodny, E. H., Bilaniuk, L. T., Wang, D. J., Assadi, M., Goldfarb, O., Goldman, H. W., Freese, A., Young, D., During, M. J., Samulski, R. J., & Janson, C. G. (2012). Long-term follow-up after gene therapy for canavan disease. Science translational medicine, 4(165), 165ra163.
  45. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  46. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  47. Traeger, E.C., & Rapin, I. (1998). The clinical course of Canavan disease. Pediatric Neurology, 18(3):207-212.
  48. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.
  49. Pleasure, D., Guo, F., Chechneva, O. et al. (2020). Pathophysiology and Treatment of Canavan Disease. Neurochem Res 45, 561–565.

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