Parkinson's Disease

Parkinson’s disease (PD) is a brain disorder characterized by progressing movement problems and irreversible damage to the brain.

Parkinson’s Disease

Parkinson’s disease is a neurodegenerative disorder that affects motor systems in early stages, leading to symptoms such as trembling, slowing of movement, and muscle stiffness. PD is also associated with autonomic nervous system and neuropsychiatric problems. Although there are several therapies available to treat the symptoms of PD, no treatments are available that halt disease progression.

Tyrosine hydroxylase staining can be used to assess dopaminergic cell loss after localized lesions in the substantia nigra.

Brain pathology: alpha-synuclein and substantia nigra degeneration

The hallmarks of Parkinson’s disease (PD) seen in post-mortem brain tissue of patients are intracellular inclusions of the protein alpha-synuclein (α-syn) termed Lewy bodies and death of cells in substantia nigra (SN). Although Lewy bodies and degeneration in the SN are related to the motor symptoms, both α-syn inclusions and neurodegeneration spread through the rest of the brain at later stages.
It is thought that lysosomal dysfunction, spreading of α-syn aggregates, and neuroinflammation are key events in the neurodegeneration and clinical symptoms observed in PD. All these disease mechanims can be modelled in different mouse models of PD.

Risk factors: SNCA, LRRK2, GBA

Mutations in the genes SNCA, LRRK2, and GBA are known to play an important role in both familial and sporadic forms of Parksinson’s disease (PD). SNCA encodes the protein alpha-synuclein, thereby providing additional evidence that this protein plays a central role in PD. LRRK2 and GBA encode proteins that play a central role in intracellular clearance pathways.
Mouse models that mimic these risk factors are therefore attractive models of PD. These models can be used to test treatments for PD.

The neurotoxin MPTP induces neuroinflammation and behavioral symptoms relevant to PD in human rodent.

Sylics offers services in transgenic mouse models that (over)express Alpha-Synuclein, leading to relevant pathology.

Sylics offers services by injecting Alpha-Synuclein protein preparation into the brain, inducing PD related pathology.

Sylics offers services with mouse models with impaired GBA enzyme function, leading to accumulation of substrates in lysosomes.

Sylics offers services with LRRK2 rodent models generated by the Michael J. Fox Foundation (MJFF).

Sylics offer services in a mouse and rat model with a specific dopaminergic lesion by local injection of 6-OHDA

Sylics offers services in a mouse model with NLRP3 inflammasome activation relevant to neuroinflammation seen in PD.

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