Anti-amyloid-β disease-modifying therapies for Alzheimer′s disease: the dawn of a new era / 中华神经科杂志

Alzheimer′s disease (AD) is the most common neurodegenerative disease. Its etiology and pathogenesis remain unclear. Since its inception, the amyloid-β (Aβ) cascade hypothesis has dominated the field of AD research and has provided the intellectual framework for disease-modifying therapies. Nowadays, many Aβ-targeted therapies have been accelerated approval or received Food and Drug Administration′s breakthrough therapy designation which offers a new dawn for disease-modifying treating AD. This article reviews the research progress of clinical trials of Aβ-targeting modification therapies, and summarizes the lessons learned from the clinical failure with several classes of anti-Aβ drugs. Although many challenges remain, anti-Aβ therapies have become a promising treatment strategy for AD.

Interferon beta-1b Treatment in a Korean Girl with Multiple Sclerosis / 대한소아신경학회지

Here we report a case of pediatric multiple sclerosis treated with interferon beta-1b. Interferon beta is widely used in adult patients with multiple sclerosis (MS). However, its effects and safety in pediatric patients have not been well established. Although supporting data are limited, the use of disease modifying therapies (DMTs) such as interferon beta-1b is recommended early in treatment of children with MS. Reports of interferon beta treatment in pediatric MS patients in Korea are rare. In this report, we describe a Korean girl who was effectively treated with interferon beta-1b for three years. There were no relapses or serious side effects. Therefore, this report provides evidence supporting the use of interferon beta in pediatric MS patients in Korea and other Asian countries. We also reviewed current medical treatment of MS, including some DMTs and second-line treatment options such as natalizumab and cyclophosphamide, and several new oral agents such as fingolimod.

Immunopathogenic Mechanism Based Treatment of Multiple Sclerosis / 한양의대학술지

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination, focal infiltration of inflammatory cells and axonal injury, which leads to loss of neurological function. The exact cause of the disease remains unclear, but an autoimmune response directed against CNS antigens is suspected. Studies in experimental autoimmune encephalomyelitis (EAE), an animal model of MS, have provided important insights into mechanisms of T cell-mediated CNS autoimmune disease. It appears likely that when a genetically susceptible host encounters a common environmental antigen (such as an infectious organism), a process called 'molecular mimicry' results in the peripheral activation of cross-reactive T cells that can migrate to the CNS and mount pro-inflammatory responses to myelin epitopes. This review describes the current understanding on the immunopathogenesis of MS and the mechanisms of action of currently available disease-modifying therapies in the context of the underlying immunopathogenic processes they are thought to affect.