TY - CHAP
T1 - RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology
T2 - A systemic overview
AU - Akhter, Firoz
AU - Akhter, Asma
AU - Kesari, Kavindra Kumar
AU - Javed, Ruheena
AU - Ruokolainen, Janne
AU - Vuorinen, Tapani
PY - 2019/1/1
Y1 - 2019/1/1
N2 - Alzheimer's disease (AD) is the most common irreversible, progressive brain disorder which causes problems with memory, thinking and behavior with the age. Alzheimer's is the sixth leading cause of death in the United States. Combination of genetic, environmental factors like; chemical radiations, toxicants and mutagens are the main causes for neurodegeneration. Including with these factors some other events can produce early stages of AD, known as early stage AD, and lead to the same eventual distinctive final pathways in the late stages. Such stages could be characterized by neuroinflammation, oxidative stress and neurodegeneration. Furthermore, advanced glycation end products (AGEs) exacerbate amyloid beta (Aβ) has shown enhanced neurotoxicity. Considering these factors, we reinvestigated the role of AGE-RAGE interaction in AD pathology. Accumulation of AGEs is a normal feature of aging, but it becomes impaied in AD. AGEs are prominent in amyloid plaques and neurofibrillary tangles. Several lines of evidences demonstrate that AGE-RAGE interactions are critical for disease pathogenesis and it is at least partially responsible for extensive oxidative stress, inflammation, and neurodegeneration. Thereforemany in vitro, in vivo and clinical studies have been focused on AGE-RAGE inhibitors, although their undesirable side effects and solubility issues may limits the usage. Therefore, it is needed to develop a potential, effective and multi-targeted inhibitors in order to prevent AGE induced neurological disorder.
AB - Alzheimer's disease (AD) is the most common irreversible, progressive brain disorder which causes problems with memory, thinking and behavior with the age. Alzheimer's is the sixth leading cause of death in the United States. Combination of genetic, environmental factors like; chemical radiations, toxicants and mutagens are the main causes for neurodegeneration. Including with these factors some other events can produce early stages of AD, known as early stage AD, and lead to the same eventual distinctive final pathways in the late stages. Such stages could be characterized by neuroinflammation, oxidative stress and neurodegeneration. Furthermore, advanced glycation end products (AGEs) exacerbate amyloid beta (Aβ) has shown enhanced neurotoxicity. Considering these factors, we reinvestigated the role of AGE-RAGE interaction in AD pathology. Accumulation of AGEs is a normal feature of aging, but it becomes impaied in AD. AGEs are prominent in amyloid plaques and neurofibrillary tangles. Several lines of evidences demonstrate that AGE-RAGE interactions are critical for disease pathogenesis and it is at least partially responsible for extensive oxidative stress, inflammation, and neurodegeneration. Thereforemany in vitro, in vivo and clinical studies have been focused on AGE-RAGE inhibitors, although their undesirable side effects and solubility issues may limits the usage. Therefore, it is needed to develop a potential, effective and multi-targeted inhibitors in order to prevent AGE induced neurological disorder.
UR - http://www.scopus.com/inward/record.url?scp=85066292160&partnerID=8YFLogxK
U2 - 10.1007/978-3-319-96511-6_9
DO - 10.1007/978-3-319-96511-6_9
M3 - Chapter
AN - SCOPUS:85066292160
SN - 978-3-319-96510-9
T3 - Environmental Science and Engineering
SP - 159
EP - 170
BT - Networking of Mutagens in Environmental Toxicology
PB - Springer
ER -