Starting with the first, and most common type, Sporadic CJD was first discovered in 1921 in Germany by Dr. Creutzfeldt. Unfortunately, we do not know what causes the protein go rogue (it is not linked to Mad Cow or any environmental factors, as of yet). Common symptoms of Sporadic CJD are dimentia, loss of balance/coordination, and hindered speech.
Variant CJD is related to Mad Cow Disease. The first cases occured in 1994, but it wasn't identified until 1996. The cause of Variant CJD is most likely due to human consumption of infected cows. The first symptoms of vCJD are mainly psychological: depression and hallucinations. A few months into the illness, neurological symptoms start to arise: memory loss and loss of muscle control.
Genetic CJD is pretty self-explanatory; the disease is passed from parents to offspring. There is a genetic mutation in the PRNP gene, that causes the protein to be irregular. This form is extremely rare and the symptoms vary from individual to individual.
And lastly, Iatrogenic CJD is acquired through a medical procedure. For example, if a donor suffers from CJD, the recipients of his organs can acquire iCJD. Thus there normal proteins are converted to rogue proteins. The most common procedures resulting in iCJD are the injection of human growth hormone and human dura mater grafts. Other procedures which are less common include corneal transplants, neurosurgery, and organ transplants.