Proteases, a class of enzymes responsible for proteolytic cleavage, play multifaceted roles in neuroscience and are important for the regulation of neuronal development, synaptic plasticity, and protein turnover in the brain. Dysregulation of proteases has been linked to various neurological disorders, including neurodegenerative diseases and neuroinflammation. During brain development, proteases play essential roles in sculpting neuronal architecture. For instance, matrix metalloproteinases (MMPs) are involved in axon guidance and neurite outgrowth by remodelling the extracellular matrix (ECM) and promoting neuronal migration. Disruptions in MMP activity have therefore been associated with abnormal neuronal connectivity and neurodevelopmental disorders like autism spectrum disorders. Proteases are also important players in synaptic plasticity. The brain-derived neurotrophic factor (BDNF) is a neurotrophin that enhances synaptic plasticity and is regulated by proteases. Tissue plasminogen activator (tPA) is involved in the conversion of plasminogen to plasmin, which then cleaves proBDNF to its active form, influencing synaptic strength and long-term potentiation (LTP). The dysregulation of tPA has therefore been implicated in memory deficits and cognitive impairments. Protein turnover is also crucial for maintaining cellular homeostasis in neurons. Proteasomes and lysosomes are the two main cellular structures responsible for protein degradation. The ubiquitin-proteasome system (UPS) selectively targets specific proteins for degradation, and malfunction of this system has been linked to neurodegenerative diseases like Alzheimer's and Parkinson's. Autophagy, a process facilitated by lysosomes, degrades, and recycles damaged organelles and protein aggregates, and its dysfunction is also implicated in various neurodegenerative disorders. In the context of neuroinflammation, proteases are also involved in immune responses and can have both beneficial and detrimental effects. Inflammatory proteases, such as caspases and calpains, contribute to the activation and regulation of immune cells in response to injury or infection. However, excessive activation of proteases can lead to neurotoxicity and tissue damage, as observed in various neuroinflammatory conditions, including multiple sclerosis and traumatic brain injury. Proteases are also strongly implicated in the pathogenesis of neurodegenerative diseases. In Alzheimer's disease, abnormal proteolytic processing of the amyloid precursor protein (APP) leads to the accumulation of amyloid-beta plaques, a hallmark of the disease. Additionally, the dysregulation of proteases involved in the degradation of tau protein likely contributes to the formation of neurofibrillary tangles, another characteristic feature of Alzheimer's. In Parkinson's disease, the accumulation of misfolded alpha-synuclein is associated with impaired proteasomal and autophagic degradation pathways, leading to the formation of Lewy bodies. Understanding the roles of proteases in neuroscience potentially allows new therapeutic avenues for neurological disorders. Targeting proteases involved in neuroinflammation could for example lead to the development of anti-inflammatory therapies for conditions such as multiple sclerosis. Modulating protease activity in neurodegenerative diseases may similarly offer a strategy to reduce the accumulation of toxic protein aggregates and slow disease progression. We offer a large product catalogue of research reagents for studying proteases, including Prostate Specific Antigen antibodies, and Prostate Specific Antigen ELISA Kits. Explore our full proteases product range below and discover more, for less.