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Parkinson’s Disease (PD) is a progressive neurodegenerative disorder primarily affecting movement due to the gradual loss of dopamine-producing neurons in the brain. Common motor symptoms include tremors, stiffness, slowness of movement, and postural instability, but the disease can also manifest in non-motor issues like cognitive decline, mood disorders, and sleep disturbances. PD impacts millions globally, with increasing prevalence in aging populations. Research is focused on developing new therapies to slow disease progression and improve quality of life.
The α-Synuclein PFF-Induced Parkinson’s Disease (PD) Model is a widely utilized preclinical model for studying the mechanisms underlying Parkinson's disease. This model involves the injection of preformed fibrils (PFFs) of α-synuclein into the brain, which triggers the aggregation of endogenous α-synuclein. This process closely mimics the pathological features of Parkinson’s, including the formation of Lewy body-like inclusions and the progressive degeneration of dopaminergic neurons in the substantia nigra.
Parkinson’s disease has been widely studied in rodent models, but reliably replicating key aspects like protein misfolding, neuroinflammation, and both motor and psychiatric symptoms has been challenging. The α-synuclein PFF-induced model overcomes these limitations by rapidly inducing α-synuclein aggregates in the rat brain, closely mimicking the pathological processes seen in humans with PD, offering a more accurate and efficient platform for studying the disease.
The 6-OHDA-induced Parkinson’s Disease model is a well-established rodent model used to study the loss of dopaminergic neurons, a hallmark of Parkinson’s disease. This neurotoxin-based model involves the selective destruction of dopamine-producing neurons in the brain, specifically in the substantia nigra and striatum, by administering 6-OHDA, which mimics the loss of dopaminergic neurons seen in human PD. Known for its rapid and reproducible effects, the 6-OHDA model is ideal for testing motor dysfunction and potential treatments but does not mimic protein aggregation, making it more suitable for studying dopaminergic degeneration.
The Acute MPTP-induced Parkinson’s Disease model is a widely used model for studying Parkinson’s disease, particularly in mice and non-human primates. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a neurotoxin that crosses the blood-brain barrier and selectively destroys dopaminergic neurons in the substantia nigra, mimicking the neurodegeneration seen in Parkinson’s patients. This model effectively replicates motor symptoms such as tremors and rigidity, and is commonly used for studying early-stage PD and testing neuroprotective therapies.
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is a neurotoxin that crosses the blood-brain barrier and selectively destroys dopaminergic neurons in the substantia nigra, mimicking the neurodegeneration seen in Parkinson’s patients. Sub-chronic MPTP/p mouse model in combination with the uricosuric agent probenecid allows a progressive and moderate loss of neurons in SNc, resembling the pathological condition observed in patients with PD.
The TG (mThy1-α-syn) Parkinson’s Disease model is a transgenic mouse model that overexpresses human α-synuclein under the control of the mThy1 promoter. This leads to the progressive accumulation of α-synuclein aggregates in neurons, replicating key features of Parkinson’s disease pathology, including Lewy body formation and motor impairments. This model is valuable for studying the long-term effects of α-synuclein aggregation, disease progression, and neurodegeneration, making it ideal for investigating the mechanisms of PD and testing potential disease-modifying therapies. The TG model also provides insight into both motor and non-motor symptoms of PD, such as cognitive decline and psychiatric disturbances.
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