An altered blood–brain barrier contributes to brain iron accumulation and neuroinflammation in the 6-OHDA rat model of Parkinson’s disease

Neuroscience ◽  
2017 ◽  
Vol 362 ◽  
pp. 141-151 ◽  
Author(s):  
Sonia Olmedo-Díaz ◽  
Héctor Estévez-Silva ◽  
Greger Orädd ◽  
Sara af Bjerkén ◽  
Daniel Marcellino ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Brain Barrier ◽  
Rat Model ◽  
Iron Accumulation ◽  
Brain Barrier ◽  
Brain Iron ◽  
Blood Brain ◽  
Altered Blood

Liposomes: Novel Drug Delivery Approach for Targeting Parkinson’s Disease

2020 ◽  
Vol 26 (37) ◽  
pp. 4721-4737 ◽  
Author(s):  
Bhumika Kumar ◽  
Mukesh Pandey ◽  
Faheem H. Pottoo ◽  
Faizana Fayaz ◽  
Anjali Sharma ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Drug Delivery ◽  
Parkinson's Disease ◽  
Side Effects ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Brain Targeting ◽  
Neural Cells ◽  
Blood Brain ◽  
The Brain

Parkinson’s disease is one of the most severe progressive neurodegenerative disorders, having a mortifying effect on the health of millions of people around the globe. The neural cells producing dopamine in the substantia nigra of the brain die out. This leads to symptoms like hypokinesia, rigidity, bradykinesia, and rest tremor. Parkinsonism cannot be cured, but the symptoms can be reduced with the intervention of medicinal drugs, surgical treatments, and physical therapies. Delivering drugs to the brain for treating Parkinson’s disease is very challenging. The blood-brain barrier acts as a highly selective semi-permeable barrier, which refrains the drug from reaching the brain. Conventional drug delivery systems used for Parkinson’s disease do not readily cross the blood barrier and further lead to several side-effects. Recent advancements in drug delivery technologies have facilitated drug delivery to the brain without flooding the bloodstream and by directly targeting the neurons. In the era of Nanotherapeutics, liposomes are an efficient drug delivery option for brain targeting. Liposomes facilitate the passage of drugs across the blood-brain barrier, enhances the efficacy of the drugs, and minimize the side effects related to it. The review aims at providing a broad updated view of the liposomes, which can be used for targeting Parkinson’s disease.

scholarly journals Blood–Brain Barrier Pathology in Alzheimer's and Parkinson's Disease: Implications for Drug Therapy

2007 ◽  
Vol 16 (3) ◽  
pp. 285-299 ◽  
Author(s):  
Brinda S. Desai ◽  
Angela J. Monahan ◽  
Paul M. Carvey ◽  
Bill Hendey
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Drug Therapy ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

Restless legs syndrome outside the blood–brain barrier – Exacerbation by domperidone in Parkinson's disease

2013 ◽  
Vol 19 (1) ◽  
pp. 92-94 ◽  
Author(s):  
S. Rios Romenets ◽  
Y. Dauvilliers ◽  
V. Cochen De Cock ◽  
B. Carlander ◽  
S. Bayard ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Brain Barrier ◽  
Restless Legs Syndrome ◽  
Brain Barrier ◽  
Restless Legs ◽  
Blood Brain

scholarly journals Blood-Brain Barrier Therapeutics for Neurological Diseases

2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Aarushi Sahni ◽  
Nicole Katchur
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Blood Brain Barrier ◽  
Neurological Diseases ◽  
Amyloid Β ◽  
Brain Barrier ◽  
Neuroinflammatory Response ◽  
Selective Filter ◽  
Blood Brain ◽  
The Brain

The Blood-Brain Barrier (BBB) is a highly selective filter responsible for allowing certain gases such as oxygen and lipid-soluble molecules to pass (Anand 2014). Its selectiveness makes it challenging for many therapeutics to combat Alzheimer’s and Parkinson’s disease with external drug therapies. Large-molecule drug therapies never pass the BBB while small-molecule drugs pass only about 5% of the time (Pardridge 2005). In Alzheimer’s disease, tight junctions between endothelial cells degrade, causing an unregulated accumulation of amyloid-β (Aβ) protein (Ramanathan 2015). Consequently, this leads to the formation of neurofibrillary tangles that cut off the nutrient supply to the brain cells and kill neurons (Ramanathan 2015). In Parkinson’s disease, astrocyte mutations cause a build-up of α-synuclein (αSyn) which affects the neuroinflammatory response and causes dysfunction in dopaminergic neurons (Booth 2017; Meade 2019). New drug therapies for Alzheimer’s and Parkinson’s continue to undergo trials; some such as FPS-ZM1 and tilavonemab for Alzheimer’s and Ravicti for Parkinson’s have shown promising results. In addition, similarities in dysfunction for both diseases and some types of cancer have sparked possibilities in retargeting cancer drugs to improve Alzheimer's and Parkinson’s pathologies. This review will summarize current therapeutic advancements for Alzheimer’s and Parkinson’s disease and their possible future contributions.

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