Group 1 - Nearly 10 million people globally suffer from Parkinson's disease, a neurodegenerative disorder characterized by the gradual death of dopamine-producing cells in the brain, leading to symptoms such as tremors, muscle stiffness, slowed movements, and balance issues [1] - Each Parkinson's patient incurs approximately $10,000 annually in direct and indirect medical costs for treatment, which remains limited and lacks a cure [2] - The scientific community has been exploring the causes of Parkinson's disease for decades, aiming to improve symptoms and potentially predict onset, with some experimental therapies showing promise in reversing symptoms [3] Group 2 - According to predictions from the British Medical Journal, the number of global Parkinson's cases could exceed 25 million by 2050, representing a 112% increase from 2021 [4] - Research led by Professor Kay Double from the University of Sydney has identified a mutated protein, SOD1, in Parkinson's patients that loses its protective function and accumulates in the brain, causing neuronal damage [5][6] - A drug named CuATSM, designed to deliver copper directly to brain tissue, is being evaluated for its efficacy in potentially reversing Parkinson's symptoms by restoring the function of the SOD1 protein [6][7] Group 3 - In a two-phase experiment, the first phase determined the optimal dosage of CuATSM, with a dosage of 15 mg per kg of body weight found to effectively increase copper levels in the brain [7] - The second phase involved genetically modified mice with Parkinson's-like symptoms, where those treated with CuATSM showed no decline in motor skills, while the placebo group did, indicating a restoration of SOD1 function and protection of dopamine neurons [8][10] - The black substance in the brain is crucial for motor control, coordination, learning, and certain cognitive functions [9] Group 4 - Research from Stanford University suggests that inhibiting the overactive LRRK2 enzyme, associated with a genetic mutation in some Parkinson's patients, may stabilize the condition, particularly in early-stage patients [11] - Approximately 25% of Parkinson's cases are attributed to genetic factors, with LRRK2 mutations being the most common [11] - Initial experiments with a compound called MLi-2 aimed at reducing LRRK2 enzyme activity did not show significant changes, but extending the treatment period to three months resulted in restored communication between dopamine neurons and the striatum [12][14] Group 5 - The restoration of primary cilia in neurons and glial cells in genetically modified mice indicated potential for repairing damaged neural circuits in Parkinson's disease [14] - The MLi-2 therapy shows great potential in repairing Parkinson's-related neural circuit activity, with ongoing clinical trials for LRRK2 inhibitors expected to translate findings from mice to human applications [14][15] - Identifying early symptoms of Parkinson's is crucial for maximizing the effectiveness of the therapy, as symptoms may appear up to fifteen years before characteristic tremors [14]