Parkinson’s disease tagged posts

Drug Delivery Technique Bypasses BBB may help many patients with Neurological Conditions

Drugs used to treat a variety of central nervous system diseases may be administered through the nose and diffused through an implanted mucosal graft (A, in red) to gain access to the brain. Under normal circumstances, there are multiple layers within the nose that block the access of pharmaceutical agents from getting to the brain including bone and the dura/arachnoid membrane, which represents part of the blood-brain barrier (B). After endoscopic skull base surgery (C), all of these layers are removed and replaced with a nasal mucosal graft, which is 1,000 times more porous than the native blood-brain barrier. Consequently, these grafts may be used to deliver very large drugs, including proteins, which would otherwise be blocked by the blood-brain barrier. Credit: Garyfallia Pagonis and Benjamin S. Bleier, M.D.

Drugs used to treat a variety of central nervous system diseases may be administered through the nose and diffused through an implanted mucosal graft (A, in red) to gain access to the brain. Under normal circumstances, there are multiple layers within the nose that block the access of pharmaceutical agents from getting to the brain including bone and the dura/arachnoid membrane, which represents part of the blood-brain barrier (B). After endoscopic skull base surgery (C), all of these layers are removed and replaced with a nasal mucosal graft, which is 1,000 times more porous than the native blood-brain barrier. Consequently, these grafts may be used to deliver very large drugs, including proteins, which would otherwise be blocked by the blood-brain barrier...

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Immune Gene Prevents Parkinson’s disease, Dementia

Highlights •Lack of neuronal IFN-β-IFNAR signaling causes brain Lewy body accumulation •IFN-β deficiency causes late-stage autophagy block and thereby α-synuclein aggregation •IFN-β promotes neuronal autophagy and α-synuclein clearance •Ifnb gene therapy prevents dopaminergic neuron loss in a familial PD model

Highlights •Lack of neuronal IFN-β-IFNAR signaling causes brain Lewy body accumulation •IFN-β deficiency causes late-stage autophagy block and thereby α-synuclein aggregation •IFN-β promotes neuronal autophagy and α-synuclein clearance •Ifnb gene therapy prevents dopaminergic neuron loss in a familial PD model

Non-inheritable PD may be caused by functional changes in the immune regulating gene Interferon-beta. Treatment with Interferon-beta-gene therapy successfully prevented neuronal death and disease effects in an experimental model of PD.

7-10 million people worldwide are living with PD. More than half of PD patients develop progressive disease showing signs of dementia similar to Alzheimer’s disease...

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Smart Immune Cells teach Neurons damaged by Parkinson’s to Heal themselves

Smart Immune Cells teach Neurons damaged by Parkinson's to Heal themselves

Smart Immune Cells teach Neurons damaged by Parkinson’s to Heal themselves

As a potential treatment for Parkinson’s disease, scientists have created smarter immune cells that produce and deliver a healing protein to the brain while also teaching neurons to begin making the protein for themselves.

The researchers, led by A/Prof Elena Batrakova at UNC Eshelman School of Pharmacy’s Center for Nanotechnology in Drug Delivery, genetically modified macrophages to produce glial cell-derived neurotrophic factor, or GDNF, and deliver it to the brain. Glial cells provide support and protection for nerve cells throughout the brain and body, and GDNF can heal and stimulate the growth of damaged neurons.

“Currently, there are no treatments that can halt or reverse the course of Parkinson’s disease...

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New Research Sheds Light on the Molecular Origins of Parkinson’s disease

 

Two gene-regulating molecules have been found to have a protective effect in the set of neurons most affected by the disease, and when their activity wanes, disease sets in. This discovery suggests new avenues by which the disease might be prevented or treated.

METHOD: They used genetically engineering mice to capture the genetic messages being translated into proteins in a specific population of cells. They then mapped the interactions of regulator genes with their target genes in the mouse brain, and used this new tool to interpret the changes they documented between normal mice and those suffering from Parkinson’s-like degeneration.

This led them to 2 molecules: proteins SATB1 and ZDHHC2, which are more abundant in the dopaminergic neurons in the SNpc (Substantia Nigra pars compac...

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