Involvement of inflammation in Alzheimer's disease pathogenesis and therapeutic potential of anti-inflammatory agents.
Alzheimer's disease (AD) is the most common form of dementia. It is characterized by beta-amyloid (Aβ) peptide fibrils, which are extracellular depositions of a specific protein, and is accompanied by extensive neuroinflammation. Various studies have demonstrated risk factors that can affect AD pathogenesis, and they include accumulation of Aβ, hyperphosphorylation of tau protein, and neuroinflammation. Among these detrimental factors, neuroinflammation has been highlighted by epidemiologic studies suggesting that use of anti-inflammatory drugs could significantly reduce the incidence of AD. Evidence suggests that astrocytes, microglia, and infiltrating immune cells from periphery might contribute to or modify the process of neuroinflammation and neurodegeneration in AD brains. In addition, recent data indicate that microRNAs may affect neuroinflammatory responses in the brain. This article focuses on supportive evidence that neuroinflammation plays a critical role in AD development. In addition, we depict putative therapeutic capacity of anti-inflammatory drugs for AD prevention or treatment. We also discuss pathogenic mechanisms by which astrocytes, microglia, T cells and microRNA participate in AD and the neuroprotective mechanisms of anti-inflammatory drugs.
College of Pharmacy, Yeungnam University, 280 Daehak-ro, Gyeongsan, Gyeongbuk, 712-749, Republic of Korea.
Sina
S
Shadfar
College of Pharmacy and Medical Research Center, Chungbuk National University, 52 Naesudong-ro, Heungdeok-gu, Cheongju, Chungbuk, 361-763, Republic of Korea.
Chul Ju
CJ
Hwang
College of Pharmacy, Yeungnam University, 280 Daehak-ro, Gyeongsan, Gyeongbuk, 712-749, Republic of Korea.
Mi-Sun
MS
Lim
College of Pharmacy, Yeungnam University, 280 Daehak-ro, Gyeongsan, Gyeongbuk, 712-749, Republic of Korea. neochallenger@yahoo.co.kr.
Dong-Young
DY
Choi
College of Pharmacy and Medical Research Center, Chungbuk National University, 52 Naesudong-ro, Heungdeok-gu, Cheongju, Chungbuk, 361-763, Republic of Korea. jinthong@chungbuk.ac.kr.
Jin Tae
JT
Hong
D000544:Alzheimer Disease / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001253:Astrocytes / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D001921:Brain / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors* / Q000276:immunology; D017628:Microglia / Q000187:drug effects / Q000276:immunology / Q000473:pathology
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators
Alzheimer’s disease; Amyloidogenesis; Anti-inflammatory; Beta-amyloid; Neuroinflammation