Parkinson's disease (PD) is a prevalent and incurable neurological illness that affects about 1% of people over 65. Although clinically defined by cardinal motor signs and pathologically defined by midbrain dopaminergic cell loss combined with intraneuronal Lewy bodies, the molecular processes underlying neurodegeneration remain unknown. It is evident that genetic variables play a role in the disease's complicated pathophysiology. The identification of illness-causing genes has made significant progress in understanding the genetic basis of this disease over the last 25 years. To date, at least 23 loci and 13 genes have been identified as being connected to hereditary forms of Parkinsonism, and genome-wide association studies have provided persuasive evidence that polymorphic variants in these genes contribute to sporadic Parkinsonism. Understanding the roles of their protein products has uncovered the neurodegenerative pathways that hereditary and sporadic Parkinson's disease may share. Impressive sets of data in different model systems strongly suggest that mitochondrial dysfunction plays a central role in clinically similar, early-onset autosomal recessive PD forms caused by parkin and PINK1 and possibly DJ-1 gene mutations. Due to mutations in SCNA and LRRK2, alpha-synuclein build up in Lewy bodies defines a spectrum of illnesses spanning from conventional late-onset PD to PD dementia, as well as sporadic and autosomal dominant PD variants. The pathogenic significance of Lewy bodies, on the other hand, is unknown because they may or may not be present in PD forms with the same LRRK2 mutation. A possible unifying pathogenic event in PD is the disruption of autophagy-based protein/organelle breakdown processes.

The critical task for the coming decade will be to strengthen these discoveries and locate other convergence sites by identifying novel genes responsible for Mendelian variants of PD, and to research their roles and interactions. In recent years, therapeutic strategies for PD have been developed in many ways. Various possibilities involving cell treatment, electrical stimulation, and neurotrophic agents are becoming a reality, including medication, surgery, rehabilitation, and other known therapies. The pathological condition of PD, animal model development, illness progression mechanisms, and therapeutic effect mechanisms of each treatment are all presented synergistically.

The aim of this Special Issue is to collect a range of novel research on the pathological condition and progression of PD and possible therapies. Researchers are invited to submit original research and review articles.

Potential topics include but are not limited to the following:

• The pathological condition and PD progression
• Emerging therapeutic strategy
• Genetics in PD
• Advancement of PD model animals
• Alternative therapies in PD
• Nonpharmacological therapies in PD
• Pros and cons of animal models in PD
• Nature-inspired synthetic derivatives in PD
• Medicinal Plants and their bioactive potential in PD