Webinars will be hosted by Dr. Pablo Villoslada (CSO).
Registration link is provided in webinar desciption.
Webinar recording will be available on demand after the webinar is over. Use the registration link to get access.
February 16th | 6pm CET/ 12pm ET/ 9am PST
Pitch: Current therapies for MS are based on anti-inflammatory drugs that partially slow the disease course. However, brain damage still progresses over time, producing increasing disability. For this reason, developing new therapies aimed to protect the brain against damage, the neuroprotective strategy, is highly expected by patients and neurologists. In this webinar, two top experts in MS will review complementary approaches to neuroprotection for MS, including targeting neuronal mechanisms of survival and trophic factors and promoting remyelination.
March 2nd | 7.30pm CET/ 1.30pm ET/ 10.30 am PST
Pitch: Testing neuroprotective and neurorepair therapies for MS is challenging because it evolves slowly over decades and has significant clinical heterogeneity. A promising approach is using acute relapses in an anatomical location such as the visual pathway that is highly eloquent and amenable for assessing its damage and recovery in MS. Acute Optic Neuritis is a common relapse of MS, damaging the visual pathway. The conjunction of recent prospective studies with the availability of very accurate imaging technologies such as Optical Coherence Tomography provides the opportunity to use this indication as a testing model for disease-modifying therapies aimed to protect the brain. Recent trials conducted in patients with Acute Optic Neuritis will be discussed.
March 8th | 5pm CET/ 11am ET/ 8am PST
Pitch: The development of disease-modifying therapies for a neurodegenerative disease like Parkinson’s disease would require modulating neurons’ proteopathy damage. Several approaches are being pursued in the case of Parkinson’s disease, a condition in which the accumulation and aggregation of alpha-synuclein (a-syn) seem to play a pivotal role. Some approaches include targeting directly a-syn with small chemicals, antibodies, or other drugs. Alternatively, modulating the activity of proteins regulating interactions with a-syn is another approach being pursued. Prolyl-Endopeptidase modulates protein aggregation, phosphorylation of a-syn, and its degradation by autophagy, becoming a promising therapeutic target for this disease.
March 30th | 5pm CET/ 11am ET/ 8am PST
Pitch: The treatment of epilepsy focused on stopping seizures by blocking ion channels and receptors, with the subsequent stopping of neuronal firing. Although this approach has achieved some degree of success, there are still significant unmet needs for people with epilepsy. Repetitive seizures and status epilepticus contribute to secondary CNS damage, worsening seizure control (refractory seizures and status epilepticus), and producing neurological disability (e.g., cognitive impairment), the epileptogenesis paradigm. The extracellular matrix’s role is critical in mediating the epileptogenic damage to worsening of seizure control and progression of permanent disability. Targeting extracellular changes.
*Date in April or May to be confirmed
Pitch: Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and many others are characterized by abnormal neuronal protein processing. Such proteopathy damage is now being pursued as a therapeutic target for slowing disease progression. However, this represents a challenge for drug discovery because it requires targeting protein-protein interactions, a young and complex field that would require a new therapeutic paradigm. In this webinar, we will discuss the role of protein-protein interactions and aggregation in neurodegenerative diseases using the case of alpha-synuclein aggregation in Parkinson’s disease. The prospects for new therapeutics for this condition based on the modulation of protein interactions and aggregation will be discussed.
April 26th | 5pm CET/ 11am ET/ 8am PST
Pitch: The role of metalloproteinase-9 (MMP-9) in neuroinflammation and brain damage has been well characterized, being critical for extracellular matrix remodeling, synapsis maintenance, homeostatic maintenance, and regulation of the blood-brain barrier. Inhibition of MMP-9 has been pursued to decrease secondary damage for many indications, including stroke, MS, epilepsy, trauma, or neurodegeneration. New approaches for targeting MMP-9 with high selectivity and enhanced penetration to the CNS will limit CNS damage and permanent disability.