Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder worldwide after Alzheimer’s disease, is pathologically characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the abnormal intracellular aggregation of α-synuclein into Lewy bodies. Traditionally, the clinical symptoms of PD have focused on motor dysfunction, which includes characteristic signs such as resting tremor, rigidity, bradykinesia, and postural instability. However, increasing evidence from both clinical and basic research suggests that the clinical presentation of PD is highly diverse, with neuropsychiatric complications representing a significant and unavoidable aspect of the disease’s overall burden. From the perspective of clinical phenotypes, the range of neuropsychiatric symptoms associated with PD is extensive, primarily including depressive disorders, generalized anxiety, apathy, impulse control disorders, and cognitive impairments related to executive function and memory. Notably, emotional and cognitive dysfunctions often manifest years prior to the onset of motor symptoms. This clinical observation indicates that the pathological processes of PD may originate within the non-motor circuits of the central nervous system (CNS), particularly in neural networks closely linked to emotional regulation and cognitive function. As one of the human body’s most lipid-rich organs, the CNS comprises lipids that account for approximately 50%-60% of the dry weight of brain tissue. These lipid molecules serve not only as structural components but also actively participate in the formation of cell membrane phospholipid bilayers, myelin sheath insulation layers, and various signal transduction complexes. From a functional perspective, lipids not only provide the structural foundation necessary for maintaining neuronal membrane fluidity, synaptic plasticity, and ion channel activity, but also act as essential molecules in energy metabolism, signal transduction, and epigenetic regulation. Notably, the frontal cortex—particularly its evolutionarily specialized prefrontal cortex (PFC)—functions as the brain’s “executive center for cognition and emotion”. This region is pivotal for higher cognitive functions, including working memory, decision-making, and behavioral inhibition, as well as for the complex regulation of emotions, such as reward and risk assessment. This region displays an exceptionally high synaptic density and is abundant in structural lipids, including unsaturated fatty acids and cholesterol, which makes it particularly vulnerable to disturbances in lipid metabolism. In PD research, lipid imbalance has become a central focus. As investigations progress, the importance of lipid metabolic pathways becomes increasingly apparent. Simultaneously, pharmacological therapies aimed at lipid regulation show considerable efficacy in addressing cognitive and emotional deficits associated with PD. In light of this, the present study utilizes bioinformatics analysis to identify differentially expressed genes in the peripheral blood of PD patients, demonstrating significant enrichment in processes such as chronic depression, cholesterol metabolism, fatty acid metabolism, AMPK signaling pathways, and insulin resistance. Expanding on this groundwork, the present review systematically explores the connections between dysregulated lipid metabolism and metabolic reprogramming in cognitive and emotional impairments associated with PD. Through the analysis findings, intervention approaches focusing on various fundamental pathological pathways such as neuroinflammation, mitochondrial dysfunction, imbalance in lactate homeostasis, and disrupted protein homeostasis are suggested. These proposals provide innovative perspectives for advancing mechanistic investigations and therapeutic advancements targeting cognitive and emotional disorders in PD.