Iron deposition in Parkinson's disease (PD) is a critical pathological feature, linked to neurodegeneration and disease progression. Abnormal iron metabolism leads to disrupted iron distribution, transport, storage, and circulation, resulting in iron accumulation in the substantia nigra (SN) and other brain regions. Excess iron induces oxidative stress, mitochondrial dysfunction, and iron-dependent cell death, exacerbating PD pathology. Iron deposition varies among PD patients, correlating with clinical symptoms and disease stages. MRI techniques such as susceptibility-weighted imaging (SWI), R2*-weighted imaging, and quantitative susceptibility mapping (QSM) are used to assess cerebral iron deposition, offering insights into PD diagnosis and progression. Iron deposition is a promising therapeutic target, but iron chelation therapy has shown mixed results in clinical trials. Iron chelators may worsen PD symptoms, highlighting the need for further research into the mechanisms of iron deposition and its impact on PD. Iron deposition is associated with α-synuclein pathology, neuroinflammation, and mitochondrial dysfunction. It also influences dopamine metabolism and contributes to non-motor symptoms. Iron deposition patterns can help differentiate PD from other neurodegenerative diseases. While iron chelation therapy shows potential, its efficacy and safety require further investigation. Overall, iron deposition plays a complex role in PD pathogenesis, involving multiple mechanisms, and remains an important area of research for developing targeted therapies.Iron deposition in Parkinson's disease (PD) is a critical pathological feature, linked to neurodegeneration and disease progression. Abnormal iron metabolism leads to disrupted iron distribution, transport, storage, and circulation, resulting in iron accumulation in the substantia nigra (SN) and other brain regions. Excess iron induces oxidative stress, mitochondrial dysfunction, and iron-dependent cell death, exacerbating PD pathology. Iron deposition varies among PD patients, correlating with clinical symptoms and disease stages. MRI techniques such as susceptibility-weighted imaging (SWI), R2*-weighted imaging, and quantitative susceptibility mapping (QSM) are used to assess cerebral iron deposition, offering insights into PD diagnosis and progression. Iron deposition is a promising therapeutic target, but iron chelation therapy has shown mixed results in clinical trials. Iron chelators may worsen PD symptoms, highlighting the need for further research into the mechanisms of iron deposition and its impact on PD. Iron deposition is associated with α-synuclein pathology, neuroinflammation, and mitochondrial dysfunction. It also influences dopamine metabolism and contributes to non-motor symptoms. Iron deposition patterns can help differentiate PD from other neurodegenerative diseases. While iron chelation therapy shows potential, its efficacy and safety require further investigation. Overall, iron deposition plays a complex role in PD pathogenesis, involving multiple mechanisms, and remains an important area of research for developing targeted therapies.