Modulating α-synuclein propagation and decomposition: Implications in Parkinson's disease therapy

Exosomes in the Diagnosis of Neuropsychiatric Diseases: A Review

“…The major pathologic change in AD is neurofibrillary tangles caused by deposition of amyloid β-protein (Aβ) and Tau proteins [ 77 ], and clinical diagnosis is made by imaging of Aβ protein deposition with positron emission tomography (PET) and/or detection of Aβ and Tau protein concentrations in CSF [ 78 , 79 ]. PD is a progressive disorder characterized by resting tremor, muscle hypertonia, bradykinesia, and, eventually, gait and postural instability; the main pathogenic mechanisms of PD are neurotoxicity caused by protein misfolding and Lewy body formation [ 80 , 81 ], progressive lesions of dopamine (DA) neurons caused by oxidative stress [ 82 ], and impaired glutamatergic transmission in the brain [ 83 ]. ALS is caused by protein folding, oxidative stress, axonal injury, and neuroinflammation leading to degeneration of muscle motor neurons [ 84 , 85 ].…”