期刊
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
卷 10, 期 2, 页码 163-174出版社
BENTHAM SCIENCE PUBL
DOI: 10.2174/187152711794480438
关键词
Alzheimer's disease; amyloid; tau; inflammation; disease-modifying drugs; anti-inflammatories
资金
- Monzino Foundation
- IRCCS Fondazione Ospedale Maggiore Policlinico
- Italian Ministry of Health
- Ing. Cesare Cusan
The two major neuropathologic hallmarks of AD are extracellular amyloid beta (A) plaques and intracellular neurofibrillary tangles (NFTs). A number of additional pathogenic mechanisms, possibly overlapping with A plaques and NFTs formation, have been described, including inflammation, oxidative damage, iron dysregulation, and alterations in cholesterol metabolism. In this review, all of these mechanisms will be discussed and treatments that are under development to interfere with these pathogenic steps will be presented. A primary goal of work in this area is identification of novel compounds that can block the course of the disease in early phases. For this reason they are currently termed disease modifying drugs. These drugs are designed to modify pathological steps leading to AD, thus acting on the evolution and progression of the disease. Some of these molecules are undergoing clinical testing whereas others are in preclinical phases of development. Several approaches have been considered, including mainly A beta deposition interference by anti-A aggregation agents, vaccination, gamma-secretase inhibition or selective A beta 42-lowering agents (SALAs), tau deposition interference by methyl thioninium chloride (MTC), and methods for reduction of inflammation and oxidative damage.
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