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Medium-chain acyl-CoA dehydrogenase (MCAD) is an enzyme that helps the body process medium-chain fatty acids, forming a key part of an animal’s metabolism. A recessive mutation to the gene ACADM causes an MCAD deficiency (MCADD). This results in a build-up of medium-chain fatty acids, causing neurological symptoms such as fatigue and seizures. In dogs, MCAD Deficiency is found in the Cavalier King Charles Spaniel.
Hereditary Necrotising Myelopathy (HNM), also known as ENM, is a hereditary neurological disorder that affects the spinal cord. It leads to degeneration of the white matter, resulting in loss of coordination and mobility. The disorder is caused by a mutation in the IBA57 gene and is inherited in an autosomal recessive manner. HNM has, so far, been observed only in the Kooikerhondje breed.
Neuronal Ceroid Lipofuscinosis (NCL) is a wide array of degenerative neurological conditions which cause progressive nerve damage, resulting in a loss of mobility and vision, and ultimately death. This variant, Neuronal Ceroid Lipofuscinosis type 8 (NCL8), is caused by a recessive mutation to the Ceroid‑Lipofuscinosis, Neuronal 8 (CLN8), and occurs in the English Setter. Other variants of NCL8 are found in the Australian Shepherd, German Shorthaired Pointer, Alpenländische Dachsbracke and Saluki.
Cerebellar Abiotrophy is a hereditary neurodegenerative disorder affecting the cerebellum. The cerebellum is the part of the brain responsible for balance, coordination, and fine motor control. In Kelpies this condition is linked to a mutation in the vacuole membrane protein 1 (VMP1) gene, which is important for neuronal maintenance and the cell’s natural clean‑up and recycling system. When this process does not work properly, nerve cells cannot maintain themselves and gradually deteriorate leading to progressive loss or improper development of Purkinje cells and other cerebellar cells involved in motor coordination. CA in the Kelpie is inherited in an autosomal recessive manner and typically becomes noticeable early in life, often from a few weeks to several months of age, though the severity and progression can vary widely.
Neuronal Ceroid Lipofuscinosis 6 (NCL6) is a hereditary neurodegenerative lysosomal storage disorder caused by mutations in the ceroid‑lipofuscinosis neuronal 6 (CLN6) gene. This defect leads to the build‑up of lipopigments, which are abnormal fatty waste substances that the body cannot break down properly. As these waste materials accumulate inside nerve cells, normal cell function becomes disrupted. Over time, neurons in the brain and retina degenerate, resulting in progressive neurological problems and loss of vision. In the Schapendoes, the condition is inherited in an autosomal recessive manner.
Neuronal Ceroid Lipofuscinosis 8 (NCL8) is a hereditary neurodegenerative lysosomal storage disorder caused by mutations in the Ceroid‑Lipofuscinosis Neuronal 8 (CLN8) gene. This defect leads to the build‑up of lipopigments, which are abnormal fatty waste substances that the body cannot break down properly. As these waste materials accumulate inside nerve cells, normal cell function becomes disrupted. Over time, neurons in the brain and retina degenerate, resulting in progressive neurological problems and loss of vision. In the Alpine Dachsbracke, the condition is inherited in an autosomal recessive manner.
Neuronal Ceroid Lipofuscinosis (NCL) is a wide array of degenerative neurological conditions which cause progressive nerve damage, resulting in a loss of mobility and vision, and ultimately death. This variant, Neuronal Ceroid Lipofuscinosis type 8 (NCL8), occurs in the Australian Shepherd and German Shorthaired Pointer. It is caused by a recessive mutation to the Ceroid‑Lipofuscinosis, Neuronal 8 (CLN8) gene. Other breeds that carry mutations for NCL8 include the English Setter, Alpenländische Dachsbracke, and Saluki.
La Distrofia Muscular de Cinturas Tipo 3 (LGMDR3) es una forma de distrofia muscular (DM) que ocurre en el perro salchicha miniatura. El trastorno causa rigidez muscular general, dificultad para comer e intolerancia al ejercicio. Es causada por una mutación recesiva en el gen SGCA.
