scholarly journals Nanomedicine for Neurodegenerative Disorders: Focus on Alzheimer’s and Parkinson’s Diseases

2021 ◽  
Vol 22 (16) ◽  
pp. 9082
Author(s):  
Keelan Jagaran ◽  
Moganavelli Singh
Keyword(s):  
Gene Therapy ◽  
Central Nervous System ◽  
Neurodegenerative Disorders ◽  
Treatment Strategy ◽  
Specific Treatment ◽  
Potential Treatment ◽  
Genome Wide ◽  
Parkinson’S Diseases ◽  
Genomic Studies ◽  
The Central Nervous System

Neurodegenerative disorders involve the slow and gradual degeneration of axons and neurons in the central nervous system (CNS), resulting in abnormalities in cellular function and eventual cellular demise. Patients with these disorders succumb to the high medical costs and the disruption of their normal lives. Current therapeutics employed for treating these diseases are deemed palliative. Hence, a treatment strategy that targets the disease’s cause, not just the symptoms exhibited, is desired. The synergistic use of nanomedicine and gene therapy to effectively target the causative mutated gene/s in the CNS disease progression could provide the much-needed impetus in this battle against these diseases. This review focuses on Parkinson’s and Alzheimer’s diseases, the gene/s and proteins responsible for the damage and death of neurons, and the importance of nanomedicine as a potential treatment strategy. Multiple genes were identified in this regard, each presenting with various mutations. Hence, genome-wide sequencing is essential for specific treatment in patients. While a cure is yet to be achieved, genomic studies form the basis for creating a highly efficacious nanotherapeutic that can eradicate these dreaded diseases. Thus, nanomedicine can lead the way in helping millions of people worldwide to eventually lead a better life.

scholarly journals Cannabidiol induces autophagy via ERK1/2 activation in neural cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Talita A. M. Vrechi ◽  
Anderson H. F. F. Leão ◽  
Ingrid B. M. Morais ◽  
Vanessa C. Abílio ◽  
Antonio W. Zuardi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Cannabis Sativa ◽  
Autophagic Flux ◽  
Neural Cells ◽  
Human Neuroblastoma ◽  
Trpv1 Receptor ◽  
The Central Nervous System ◽  
Catabolic Process

AbstractAutophagy is a lysosomal catabolic process essential to cell homeostasis and is related to the neuroprotection of the central nervous system. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid present in Cannabis sativa. Many therapeutic actions have been linked to this compound, including autophagy activation. However, the precise underlying molecular mechanisms remain unclear, and the downstream functional significance of these actions has yet to be determined. Here, we investigated CBD-evoked effects on autophagy in human neuroblastoma SH-SY5Y and murine astrocyte cell lines. We found that CBD-induced autophagy was substantially reduced in the presence of CB1, CB2 and TRPV1 receptor antagonists, AM 251, AM 630 and capsazepine, respectively. This result strongly indicates that the activation of these receptors mediates the autophagic flux. Additionally, we demonstrated that CBD activates autophagy through ERK1/2 activation and AKT suppression. Interestingly, CBD-mediated autophagy activation is dependent on the autophagy initiator ULK1, but mTORC1 independent. Thus, it is plausible that a non-canonical pathway is involved. Our findings collectively provide evidence that CBD stimulates autophagy signal transduction via crosstalk between the ERK1/2 and AKT kinases, which represent putative regulators of cell proliferation and survival. Furthermore, our study sheds light on potential therapeutic cannabinoid targets that could be developed for treating neurodegenerative disorders.

scholarly journals Small GTPases of the Rab and Arf Families: Key Regulators of Intracellular Trafficking in Neurodegeneration

2021 ◽  
Vol 22 (9) ◽  
pp. 4425
Author(s):  
Alazne Arrazola Arrazola Sastre ◽  
Miriam Luque Luque Montoro ◽  
Hadriano M. Lacerda ◽  
Francisco Llavero ◽  
José L. Zugaza
Keyword(s):  
Membrane Trafficking ◽  
Neurodegenerative Disorders ◽  
Synaptic Vesicles ◽  
Intracellular Trafficking ◽  
Small Gtpases ◽  
Constant Flow ◽  
Parkinson’S Diseases ◽  
The Central Nervous System ◽  
Arf Gtpases

Small guanosine triphosphatases (GTPases) of the Rab and Arf families are key regulators of vesicle formation and membrane trafficking. Membrane transport plays an important role in the central nervous system. In this regard, neurons require a constant flow of membranes for the correct distribution of receptors, for the precise composition of proteins and organelles in dendrites and axons, for the continuous exocytosis/endocytosis of synaptic vesicles and for the elimination of dysfunctional proteins. Thus, it is not surprising that Rab and Arf GTPases have been associated with neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Both pathologies share characteristics such as the presence of protein aggregates and/or the fragmentation of the Golgi apparatus, hallmarks that have been related to both Rab and Arf GTPases functions. Despite their relationship with neurodegenerative disorders, very few studies have focused on the role of these GTPases in the pathogenesis of neurodegeneration. In this review, we summarize their importance in the onset and progression of Alzheimer’s and Parkinson’s diseases, as well as their emergence as potential therapeutical targets for neurodegeneration.

scholarly journals Targeting innate immunity for neurodegenerative disorders of the central nervous system

2016 ◽  
Vol 138 (5) ◽  
pp. 653-693 ◽  
Author(s):  
Katrin I. Andreasson ◽  
Adam D. Bachstetter ◽  
Marco Colonna ◽  
Florent Ginhoux ◽  
Clive Holmes ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Innate Immunity ◽  
Nervous System ◽  
Neurodegenerative Disorders ◽  
The Central Nervous System

ANTICHOLINERGIC POISONING: TREATMENT WITH PHYSOSTIGMINE

PEDIATRICS ◽  
1973 ◽  
Vol 52 (3) ◽  
pp. 449-451
Author(s):  
Barry H. Rumack
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acetic Acid ◽  
Specific Treatment ◽  
Signs And Symptoms ◽  
The Body ◽  
Sweat Glands ◽  
Exocrine Glands ◽  
Anticholinergic Syndrome ◽  
The Central Nervous System

The increased incidence of poisoning by overdoses of commonly used drugs with anticholinergic properties (Table I) and the general lack of knowledge concerning a specific treatment for these poisons warrants a summary of the problem at this time. Some plants containing anticholinergic alkaloids are also included in this group as they may also be taken intentionally or accidentally. Drugs with anticholinergic properties primanly antagonize acetylcholine competitively at the neuroreceptor site. Cardiac muscle, exocrine glands, and smooth muscle are most markedly affected.1 Action of the inhibitors is overcome by increasing the level of acetylcholine naturally generated in the body through inhibiting the enzyme (choline esterase) which normally prevents accumulation of excess acetylcholine. It does this by hydrolyzing that compound to inactive acetic acid and choline. Agents which inhibit this enzyme, so that acetylcholine accumulates at the neuroreceptor sites, are called anticholine esterases. Physostigmine, one of the anticholine esterases which is a tertiary amine, crosses into the central nervous system and can reverse both central and peripheral anticholinergic actions2. Neostigmine and pyridostigmine are also anticholine esterases but they are quaternary amines and are capable of acting only outside the central nervous system because of solubility and ionization characteristics. The anticholinergic syndrome has both central and peripheral signs and symptoms. Central toxic effects include anxiety, delirium, disorientation, hallucinations, hyperactivity, and seizures.2 Severe poisoning may produce coma, medullary paralysis, and death. Peripheral taxicity is characterized by tachycardia, hyperpyrexia, mydriasis, vasodilatation, urinary retention, diminution of gastrointestinal motility, decrease of secretion in salivary and sweat glands, and loss of secretions in the pharynx, bronchi, and nasal passages.

Clinical Applications

2016 ◽  
pp. 236-252
Author(s):  
Elson L. So
Keyword(s):  
Intensive Care Unit ◽  
Central Nervous System ◽  
Nervous System ◽  
Specific Treatment ◽  
Clinical Problem ◽  
Clinical Applications ◽  
Neural Function ◽  
Central Nervous System Disorders ◽  
Progression Of Disease ◽  
The Central Nervous System

Many electrophysiological assessment and techniques of clinical neurophysiology can be used in the assessment of patients with suspected disease of the central nervous system. Each of the techniques is applied either to assist clinicians in assessing disease of the central nervous system or, less commonly, to monitor changes in neural function. These techniques can be used to monitor neural function in observing progression of disease, such as the frequency of seizures, or improvement in a patient’s condition with specific treatment. They are also used in the intensive care unit and operating room to identify progressive neural damage. The clinical neurophysiological testing technique that is most appropriate for a patient depends on the clinical problem, and, often, some combination of techniques best provides the necessary data. This chapter focuses on the application of clinical neurophysiological techniques in assessing patients with suspected central nervous system disorders.

The Neuroimmune Interface in Prion Diseases

Physiology ◽  
2000 ◽  
Vol 15 (5) ◽  
pp. 250-255
Author(s):  
Michael A. Klein ◽  
Adriano Aguzzi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Immune System ◽  
Prion Disease ◽  
Neurodegenerative Disorders ◽  
Prion Diseases ◽  
The Central Nervous System

Prion diseases are fatal neurodegenerative disorders of animals and humans. Here we address the role of the immune system in the spread of prions from peripheral sites to the central nervous system and its potential relevance to iatrogenic prion disease.

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