Jakob Creutzfeldt Disease (CJD) is a rare and degenerative neurological disorder that affects the brain and nervous system. Named after the German scientists Hans Gerhard Creutzfeldt and Alfons Maria Jakob who first described the disease in the 1920s, it belongs to a family of diseases known as transmissible spongiform encephalopathies (TSEs).
CJD is characterized by the accumulation of abnormal protein structures called prions within brain tissue, leading to the destruction of neurons. This abnormal protein build-up results in progressive and fatal neurological symptoms. The disease has several subtypes, including sporadic, familial, and acquired forms. Sporadic CJD is the most common form, occurring spontaneously without any known cause. Familial CJD is caused by a gene mutation inherited from one or both parents. Acquired CJD is extremely rare and occurs through exposure to contaminated tissues or medical procedures.
Symptoms of CJD typically include rapidly progressing dementia, memory loss, behavioral changes, coordination and balance problems, muscle stiffness, and visual disturbances. As the disease progresses, individuals may also experience involuntary muscle jerks, severe confusion, and difficulty speaking or swallowing.
Diagnosis of CJD can be challenging due to its rarity and similarity to other neurological conditions. It often involves clinical evaluation, neurological exams, medical history assessment, and specialized tests such as electroencephalography (EEG) and cerebrospinal fluid analysis. Currently, there is no cure for CJD, and treatment focuses on symptom management and supportive care to improve the patient's quality of life.
Due to its rare occurrence, CJD has raised concerns about its potential for transmission and public health impacts. Stringent infection control measures are in place to prevent the accidental spread of CJD
