RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology: A systemic overview

Research output: Chapter in Book/Report/Conference proceedingChapterScientificpeer-review

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RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology : A systemic overview. / Akhter, Firoz; Akhter, Asma; Kesari, Kavindra Kumar; Javed, Ruheena; Ruokolainen, Janne; Vuorinen, Tapani.

Networking of Mutagens in Environmental Toxicology. Springer Berlin Heidelberg, 2019. p. 159-170 (Environmental Science and Engineering).

Research output: Chapter in Book/Report/Conference proceedingChapterScientificpeer-review

Harvard

Akhter, F, Akhter, A, Kesari, KK, Javed, R, Ruokolainen, J & Vuorinen, T 2019, RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology: A systemic overview. in Networking of Mutagens in Environmental Toxicology. Environmental Science and Engineering, Springer Berlin Heidelberg, pp. 159-170. https://doi.org/10.1007/978-3-319-96511-6_9

APA

Akhter, F., Akhter, A., Kesari, K. K., Javed, R., Ruokolainen, J., & Vuorinen, T. (2019). RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology: A systemic overview. In Networking of Mutagens in Environmental Toxicology (pp. 159-170). (Environmental Science and Engineering). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-319-96511-6_9

Vancouver

Akhter F, Akhter A, Kesari KK, Javed R, Ruokolainen J, Vuorinen T. RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology: A systemic overview. In Networking of Mutagens in Environmental Toxicology. Springer Berlin Heidelberg. 2019. p. 159-170. (Environmental Science and Engineering). https://doi.org/10.1007/978-3-319-96511-6_9

Author

Akhter, Firoz ; Akhter, Asma ; Kesari, Kavindra Kumar ; Javed, Ruheena ; Ruokolainen, Janne ; Vuorinen, Tapani. / RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology : A systemic overview. Networking of Mutagens in Environmental Toxicology. Springer Berlin Heidelberg, 2019. pp. 159-170 (Environmental Science and Engineering).

Bibtex - Download

@inbook{7e98e658e5874561b2de593a8d136531,
title = "RAGE exacerbate amyloid beta (Aβ) induced alzheimer pathology: A systemic overview",
abstract = "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.",
author = "Firoz Akhter and Asma Akhter and Kesari, {Kavindra Kumar} and Ruheena Javed and Janne Ruokolainen and Tapani Vuorinen",
year = "2019",
month = "1",
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doi = "10.1007/978-3-319-96511-6_9",
language = "English",
isbn = "978-3-319-96510-9",
series = "Environmental Science and Engineering",
publisher = "Springer Berlin Heidelberg",
pages = "159--170",
booktitle = "Networking of Mutagens in Environmental Toxicology",

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RIS - Download

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

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T3 - Environmental Science and Engineering

SP - 159

EP - 170

BT - Networking of Mutagens in Environmental Toxicology

PB - Springer Berlin Heidelberg

ER -

ID: 35133514