The lead time for developing custom neurological disease models can vary depending on the complexity of the genetic modifications and the specific disease. For less common conditions like frontotemporal dementia, we typically require 6 to 12 months from project initiation to delivery, assuming standard genetic engineering techniques are used. Complex models might take longer. We encourage early consultation to discuss project specifics and timelines.

Yes, models like EAE for MS or LPS-induced neuroinflammation models are used to study neuroinflammation. These models allow for testing anti-inflammatory drugs by assessing reductions in immune cell infiltration, cytokine levels, and lesion formation. Optimization includes selecting strains with more robust or specific inflammatory responses to better mimic human conditions.

Our MS models, like EAE (Experimental Autoimmune Encephalomyelitis), are validated through clinical scoring of neurological deficits, histopathological examination for demyelination, and immune cell infiltration. These models mimic the inflammatory and demyelinating aspects of MS, though with less chronicity or remission-relapse patterns typical of human MS.

Our ALS models include those with mutations like SOD1, TDP-43, and C9orf72, common in human ALS. While these models don't capture the full spectrum of human genetic diversity, they reflect key genetic mechanisms. This allows for testing drug efficacy against specific genetic backgrounds, which can be crucial for personalized medicine approaches in ALS research.

For Huntington's disease, we can customize models by modulating CAG repeat length in the huntingtin gene to reflect different severity levels seen in humans. We can also introduce specific mutations or use conditional knockouts to study regional or temporal effects of the disease. Customization can focus on different aspects like onset age, progression rate, or specific symptoms.

We offer several models for Parkinson's disease research, including the α-synuclein overexpression model, which replicates Lewy body pathology, and models with mutations in genes such as LRRK2, PINK1, and Parkin. These models show motor deficits, dopaminergic neuron loss, and protein aggregation similar to human Parkinson's pathology, albeit with species-specific differences.