scholarly journals Curcumin-Loaded Nanoparticles Based on Amphiphilic Hyaluronan-Conjugate Explored as Targeting Delivery System for Neurodegenerative Disorders

2020 ◽  
Vol 21 (22) ◽  
pp. 8846
Author(s):  
Giuseppe Pepe ◽  
Enrica Calce ◽  
Valentina Verdoliva ◽  
Michele Saviano ◽  
Vittorio Maglione ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Delivery System ◽  
Neurodegenerative Disorders ◽  
Natural Polysaccharide ◽  
Promising Therapeutic Approach ◽  
Targeting Delivery ◽  
Effective Delivery ◽  
Vitro Model

Identification of molecules able to promote neuroprotective mechanisms can represent a promising therapeutic approach to neurodegenerative disorders including Huntington’s disease. Curcumin is an antioxidant and neuroprotective agent, even though its efficacy is limited by its poor absorption, rapid metabolism, systemic elimination, and limited blood–brain barrier (BBB) permeability. Herein, we report on novel biodegradable curcumin-containing nanoparticles to favor the compound delivery and potentially enhance its brain bioavailability. The prepared hyaluronan-based materials able to self-assemble in stable spherical nanoparticles, consist of natural fatty acids chemically conjugated to the natural polysaccharide. The aim of this study is to provide a possible effective delivery system for curcumin with the expectation that, after having released the drug at the specific site, the biopolymer can degrade to nontoxic fragments before renal excretion, since all the starting materials are provided by natural resource. Our findings demonstrate that curcumin-encapsulated nanoparticles enter the cells and reduce their susceptibility to apoptosis in an in vitro model of Huntington’s disease.

Neuroprotective effect of neural stem cell-conditioned media in in vitro model of Huntington's disease

2008 ◽  
Vol 435 (3) ◽  
pp. 175-180 ◽  
Author(s):  
Heon-Chang Lim ◽  
Soon-Tae Lee ◽  
Kon Chu ◽  
Kyung Min Joo ◽  
Lami Kang ◽  
...  
Keyword(s):  
Stem Cell ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Neural Stem Cell ◽  
In Vitro Model ◽  
Neuroprotective Effect ◽  
Conditioned Media ◽  
Vitro Model

MicroRNA-27a reduces mutant hutingtin aggregation in an in vitro model of Huntington's disease

2017 ◽  
Vol 488 (2) ◽  
pp. 316-321 ◽  
Author(s):  
Jae-Jun Ban ◽  
Jin-Young Chung ◽  
Mijung Lee ◽  
Wooseok Im ◽  
Manho Kim
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Neuroprotective potential of CB1 receptor agonists in an in vitro model of Huntington's disease

2010 ◽  
Vol 160 (3) ◽  
pp. 747-761 ◽  
Author(s):  
EL Scotter ◽  
CE Goodfellow ◽  
ES Graham ◽  
M Dragunow ◽  
M Glass
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
In Vitro Model ◽  
Cb1 Receptor ◽  
Receptor Agonists ◽  
Vitro Model

B01 In vitro study of neurodevelopment in huntington’s disease

2021 ◽  
Author(s):  
Phil Sanders ◽  
Waseem Abbas ◽  
Anna Esteve-Codina ◽  
Gustavo Rodriguez-Esteban ◽  
Georgina Bombau ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
In Vitro Study ◽  
Vitro Study

scholarly journals The MID1 Protein: A Promising Therapeutic Target in Huntington’s Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Annika Heinz ◽  
Judith Schilling ◽  
Willeke van Roon-Mom ◽  
Sybille Krauß
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Protein A ◽  
Cag Repeat ◽  
Cag Repeats ◽  
Progressive Movement ◽  
Promising Therapeutic Target ◽  
Promising Therapeutic Approach ◽  
Exon 1 ◽  
Polyglutamine Protein

Huntington’s disease (HD) is caused by an expansion mutation of a CAG repeat in exon 1 of the huntingtin (HTT) gene, that encodes an expanded polyglutamine tract in the HTT protein. HD is characterized by progressive psychiatric and cognitive symptoms associated with a progressive movement disorder. HTT is ubiquitously expressed, but the pathological changes caused by the mutation are most prominent in the central nervous system. Since the mutation was discovered, research has mainly focused on the mutant HTT protein. But what if the polyglutamine protein is not the only cause of the neurotoxicity? Recent studies show that the mutant RNA transcript is also involved in cellular dysfunction. Here we discuss the abnormal interaction of the mutant HTT transcript with a protein complex containing the MID1 protein. MID1 aberrantly binds to CAG repeats and this binding increases with CAG repeat length. Since MID1 is a translation regulator, association of the MID1 complex stimulates translation of mutant HTT mRNA, resulting in an overproduction of polyglutamine protein. Thus, blocking the interaction between MID1 and mutant HTT mRNA is a promising therapeutic approach. Additionally, we show that MID1 expression in the brain of both HD patients and HD mice is aberrantly increased. This finding further supports the concept of blocking the interaction between MID1 and mutant HTT mRNA to counteract mutant HTT translation as a valuable therapeutic strategy. In line, recent studies in which either compounds affecting the assembly of the MID1 complex or molecules targeting HTT RNA, show promising results.

scholarly journals Cerebral dopamine neurotrophic factor (CDNF) protects against quinolinic acid-induced toxicity in in vitro and in vivo models of Huntington’s disease

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
P. Stepanova ◽  
V. Srinivasan ◽  
D. Lindholm ◽  
M. H. Voutilainen
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Quinolinic Acid ◽  
Neurotrophic Factor ◽  
Striatal Neurons ◽  
In Vivo Models ◽  
Cerebral Dopamine Neurotrophic Factor ◽  
Cerebral Dopamine

Abstract Huntington’s disease (HD) is a neurodegenerative disorder with a progressive loss of medium spiny neurons in the striatum and aggregation of mutant huntingtin in the striatal and cortical neurons. Currently, there are no rational therapies for the treatment of the disease. Cerebral dopamine neurotrophic factor (CDNF) is an endoplasmic reticulum (ER) located protein with neurotrophic factor (NTF) properties, protecting and restoring the function of dopaminergic neurons in animal models of PD more effectively than other NTFs. CDNF is currently in phase I–II clinical trials on PD patients. Here we have studied whether CDNF has beneficial effects on striatal neurons in in vitro and in vivo models of HD. CDNF was able to protect striatal neurons from quinolinic acid (QA)-induced cell death in vitro via increasing the IRE1α/XBP1 signalling pathway in the ER. A single intrastriatal CDNF injection protected against the deleterious effects of QA in a rat model of HD. CDNF improved motor coordination and decreased ataxia in QA-toxin treated rats, and stimulated the neurogenesis by increasing doublecortin (DCX)-positive and NeuN-positive cells in the striatum. These results show that CDNF positively affects striatal neuron viability reduced by QA and signifies CDNF as a promising drug candidate for the treatment of HD.

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