The typical progression of Huntington's disease is as follows: The first symptoms are mild and begin in childhood. These may include difficulty swallowing, difficulty eating or drinking, constipation or diarrhoea, and difficulty walking, although there are several other common, everyday symptoms as well. There are many types of Huntington's disease, although all have a genetic component, and they are typically divided into two different groups: autosomal dominant Huntington's disease and heterologous Huntington's disease.
The genetic cause of ADH5 is unknown. ADH5 mutations are known to exist in two other types of inherited neurodegenerative diseases that are also associated with the ADH5 gene, ALS and familial forms of Alzheimer. Several types of ADH5-tumor cells exist, including those that are primary myelogenous, primary neuronal, and primary glioma cells. The alfacalcidol myelogenous ADH5 tumors are found predominantly in the brains of people with Parkinson's disease, but also sometimes in other cases of ALS and familial forms of Alzheimer.
Familial forms of ADH5 The ADH5 proteins are expressed in only a few types of myeloid leukemia cells. In these tumors, normal ADH5 and other proteins are not produced. These tumors do not have the normal level of ADH5 or other toxins in the bloodstream, and the tumors contain more ADH5 than the cells normal or diseased. Huntington's disease and ALS The molecularly normal and molecularly abnormal cells in the tumor and in the patients are of a somewhat different type. In the patient with familial forms of Alzheimer, the normal and normal ADH5 and some other molecules are produced, but this is not the case in patients with Huntington's disease. In patients with Huntington's disease, a significant percentage of the ADH5-positive cells also have the genetic defect known as beta-amyloidosis. The mutated enzyme is not as efficient in purging beta-amyloid, and the cells become more sensitive to beta-amyloid.