Neurodegeneration: A question of balance

  title={Neurodegeneration: A question of balance},
  author={Leslie M. Thompson},
When a disease-associated gene is mutated, is the cellular activity of its protein product enhanced or reduced? For at least one neurodegenerative disease, spinocerebellar ataxia 1, the answer seems to be both. 
Herbal Medicines Used for Neurodegenerative Diseases
The isolation of specific phytoconstituents from ethanopharmacologically important plants may lead to identification of novel neuroprotective agents or neurotonic agents.
The Impact of Natural Compounds on the Treatment of Neurodegenerative Diseases
The pathogenesis, symptoms, potential targets, treatment and natural compounds effective in the treatment of AD, PD, HD, ALS, SCA3, SBMA and CJD are discussed.
Cholesterol homeostasis: a key to prevent or slow down neurodegeneration
Some of the main results reported in the recent years in this field are critically discussed, mainly focusing on the mechanisms that, by recovering perturbations of cholesterol homeostasis in neuronal cells, may correct clinically relevant features occurring in different neurodegenerative disorders.
Dietary curcumin: a potent natural polyphenol for neurodegenerative diseases therapy
Conceptual information about the multiple potentials of curcumin for prevention and/ or treatment of neurodegenerative diseases is provided.
Tissue-Specific Upregulation of Drosophila Insulin Receptor (InR) Mitigates Poly(Q)-Mediated Neurotoxicity by Restoration of Cellular Transcription Machinery
This study demonstrates for the first time that targeted upregulation of InR could effectively mitigate poly(Q)-mediated neurodegeneration in fly models and suggests that modulation of the insulin signalling pathway could be an effective therapeutic intervention against poly( Q) disorders.
Neurodegenerative Disease Conditions and Genomic Treatment for Better Health
In this chapter, Alzheimer's disease (AD), Parkinson’s disease (PD), Huntington’S disease (HD), and amyotrophic lateral sclerosis (ALS) are discussed in detail for their pathophysiology, etiology, and latest symptomatic and preventive treatment.
Interleukin-18 promoter polymorphisms and idiopathic Parkinson disease: an Egyptian study
Polymorphisms of IL-18 gene promoter increase the risk of developing idiopathic PD, and the polymorphisms may affect phenotypic expression rather than being a direct cause of idiopATHic PD.
Deciphering the function and regulation of microRNAs in Alzheimer's disease and Parkinson's disease.
The evidence for the functional role of dysregulated miRNAs involved in disease pathogenesis, as well as how mi RNAs govern neuronal functions either upstream or downstream of target genes that are disease pathogenic factors are reviewed.
Neurodegenerative Diseases: Regenerative Mechanisms and Novel Therapeutic Approaches
The current review summarized the most common features of major neurodegenerative disorders; their causes and consequences and proposed novel therapeutic approaches.


Polyglutamine diseases: emerging concepts in pathogenesis and therapy.
This article reviews the emerging concepts in pathogenesis and therapy of polyglutamine diseases and the role of proteolytic cleavage, the importance of conformational change in the pathogenic proteins, the roles of protein aggregation and the importanceof transcriptional and metabolic disturbances.
Multiple pathways contribute to the pathogenesis of Huntington disease
The widespread expression and localization of mutant htt and its interactions with a variety of proteins suggest that mutant htt engages multiple pathogenic pathways, which will help to elucidate the pathogenesis of HD and to target therapies effectively.
Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1
It is shown that the expanded polyglutamine tract differentially affects the function of the host protein in the context of different endogenous protein complexes, contributing to SCA1 neuropathology by means of a gain-of-function mechanism.
Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration
It is demonstrated that high-throughput screening for protein interactions combined with genetic validation in a model organism is a powerful approach for identifying novel candidate modifiers of polyglutamine toxicity.
Trinucleotide repeat disorders.
It is exciting that within a span of 15 years, pathogenesis studies of this class of disorders are beginning to reveal pathways that are potential therapeutic targets.
Transgenic Mice in the Study of Polyglutamine Repeat Expansion Diseases
Analysis of patient material and other transgenic lines has now shown NII to be a common feature of all of these diseases, and in the transgenic models, inclusions are present prior to the onset of symptoms suggesting a causal relationship.
Widespread Disruption of Repressor Element-1 Silencing Transcription Factor/Neuron-Restrictive Silencer Factor Occupancy at Its Target Genes in Huntington's Disease
The same molecular phenotype is produced in cells and brain tissue depleted of endogenous huntingtin, thereby directly validating the loss-of-function hypothesis of HD, and suggesting that relief of REST/NRSF mediated repression can restore aberrant neuronal gene transcription in HD.