Canine α-synuclein antibody and antigen (recombinant protein)

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Diagnostic anti-Canine α-synuclein antibodies pairs and antigen for animal health (animal Dog/Canine Alzheimer Disease(AD)) testing in ELISA, colloidal gold-based Lateral flow immunoassay (LFIA), CLIA, TINIA and POCT

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Target/Biomarker Information

Canine α-synuclein, an evolutionary kin of its human counterpart, emerges as a fascinating player in the intricate symphony of the canine nervous system. At its core, this protein is an intrinsically disordered marvel, defying traditional structural classifications. Structurally, it bears resemblance to a "Janus-faced" molecule, with its N-terminal portion embracing amphipathic tendencies, a hydrophobic central domain, and an acidic, largely negatively charged C-terminal tail. This unique structure hints at its multifunctionality within the neuronal milieu.

Canine α-synuclein's primary residence is in the central nervous system, where it assumes an array of roles. Among its most noteworthy functions is its involvement in the regulation of synaptic vesicle dynamics. It dynamically associates with synaptic vesicles, modulating their trafficking and neurotransmitter release. This role positions Canine α-synuclein as a key player in the finely tuned orchestra of synaptic transmission.

Beyond the mechanics of neurotransmission, Canine α-synuclein partakes in the orchestration of synaptic plasticity, a fundamental process underpinning learning and memory. Its presence influences synaptic strength and the molecular cascades that contribute to adaptive changes in neural circuits. This dynamic role positions Canine α-synuclein as a molecular conductor of cognitive processes in dogs.

Yet, the intrigue surrounding Canine α-synuclein deepens as we explore its darker side—the propensity to aggregate. Much like its human counterpart, Canine α-synuclein can undergo conformational changes that lead to the formation of insoluble protein aggregates, famously known as Lewy bodies. These aggregates are central to the pathogenesis of neurodegenerative disorders, particularly in elderly dogs. The exact triggers and mechanisms governing this transition into aggregation-prone states are areas of intense research. Understanding these processes is instrumental in uncovering potential therapeutic targets to mitigate the devastating effects of neurodegenerative diseases in dogs.

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