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Disease mechanism, biomarker and therapeutics for spinal and bulbar muscular atrophy (SBMA)

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Spinal and bulbar muscular atrophy (SBMA) is a hereditary neuromuscular disorder caused by CAG trinucleotide expansion in the gene encoding the androgen receptor (AR). In the central nervous system, lower motor neurons are selectively affected, whereas pathology of patients and animal models

Retinoid analogs and polyphenols as potential therapeutics for age-related macular degeneration

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Age-related macular degeneration (AMD) is a devastating retinal degenerative disease. Epidemiological reports showed an expected increasing prevalence of AMD in the near future. The only one existing FDA-approved pharmacological treatment involves an anti-vascular endothelial growth factor (VEGF)

Wallerian degeneration as a therapeutic target in traumatic brain injury.

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Diffuse or traumatic axonal injury is one of the principal pathologies encountered in traumatic brain injury (TBI) and the resulting axonal loss, disconnection, and brain atrophy contribute significantly to clinical morbidity and disability. The seminal discovery of the slow Wallerian

Cytoplasmic ATM protein kinase: an emerging therapeutic target for diabetes, cancer and neuronal degeneration.

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Ataxia-telangiectasia (A-T) is an autosomal recessive disorder characterized by cerebellar ataxia and oculocutaneous telangiectasias. The gene mutated in this disease, Atm (A-T mutated), encodes a serine/threonine protein kinase that has been traditionally considered to be a nuclear protein

MicroRNA as Therapeutics for Age-Related Macular Degeneration.

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MicroRNA (miRNA) are a class of endogenously expressed small non-coding RNA molecules that function by repressing or silencing post-transcriptional gene expression. While miRNAs were only identified in humans as recently as the turn of this century, some miRNA-based agents are already in Phase 2

Dry age-related macular degeneration: mechanisms, therapeutic targets, and imaging.

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Age-related macular degeneration is the leading cause of irreversible visual dysfunction in individuals over 65 in Western Society. Patients with AMD are classified as having early stage disease (early AMD), in which visual function is affected, or late AMD (generally characterized as either "wet"

Therapeutic advances in 5q-linked spinal muscular atrophy.

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Spinal muscular atrophy (SMA) is a severe and clinically-heterogeneous motor neuron disease caused, in most cases, by a homozygous mutation in the SMN1 gene. Regarding the age of onset and motor involvement, at least four distinct clinical phenotypes have been recognized. This clinical variability

Therapeutic effect of psoralen on muscle atrophy induced by tumor necrosis factor-α.

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To observe and determine the effect and mechanism of psoralen on tumor necrosis factor-α (TNF-α)-induced muscle atrophy.Three sets of C2C12 cells, including blank control, TNF-α (10 or 20 ng/ml) treatment and a TNF-α (10 or 20 ng/ml) plus psoralen (80 μM)

Invertebrate models of spinal muscular atrophy: insights into mechanisms and potential therapeutics.

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Invertebrate genetic models with their tractable neuromuscular systems are effective vehicles for the study of human nerve and muscle disorders. This is exemplified by insights made into spinal muscular atrophy (SMA) using the fruit fly Drosophila melanogaster and the nematode worm Caenorhabditis

DcpS as a therapeutic target for spinal muscular atrophy.

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Spinal muscular atrophy (SMA) is caused by deletion or mutation of both copies of the SMN1 gene, which produces an essential protein known as SMN. The severity of SMA is modified by variable copy number of a second gene,SMN2, which produces an mRNA that is incorrectly spliced with deletion of the

Erythropoietin as a novel therapeutic agent for atrophic age-related macular degeneration.

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The purpose of this article is to propose a novel therapeutic approach to the treatment of age-related macular degeneration (ARMD), the leading cause of blindness in the elderly population (over 60 years of age) in developed countries. Although recent advances have been made in the treatment of the

Spinal muscular atrophy disease: a literature review for therapeutic strategies.

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Currently, there is no cure for the treatment of spinal muscular atrophy (SMA). Based on the available clinical and molecular findings, different therapeutic strategies were tested in vitro and in vivo and clinical trials are ongoing. The main therapeutic direction is focused on the enhancement of

Is spinal muscular atrophy a disease of the motor neurons only: pathogenesis and therapeutic implications?

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Spinal muscular atrophy (SMA) is a genetic neurological disease that causes infant mortality; no effective therapies are currently available. SMA is due to homozygous mutations and/or deletions in the survival motor neuron 1 gene and subsequent reduction of the SMN protein, leading to the death of

Histamime Receptor H4 as a New Therapeutic Target for Age-related Macular Degeneration.

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Histamine receptor H4 (HRH4) is one of four known histamine receptors, among which H1 receptor is primarily involved in typeI allergic reactions and H2 receptor is generally recognized for its role in gastric acid secretion. Compared with H1 and H2, HRH4 has unique characteristics; it is expressed

Pathogenic mechanisms and therapeutic strategies in spinobulbar muscular atrophy.

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We review the genetic and clinical features of spinobulbar muscular atrophy (SBMA), a progressive neuromuscular disorder caused by a CAG/glutamine tract expansion in the androgen receptor. SBMA was the first polyglutamine disease to be discovered, and we compare and contrast it with related

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