Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression

被引：90

作者：

Andronie-Cioara, Felicia Liana ^{[1
]}

Ardelean, Adriana Ioana ^{[2
]}

Nistor-Cseppento, Carmen Delia ^{[1
]}

Jurcau, Anamaria ^{[1
]}

Jurcau, Maria Carolina ^{[3
]}

Pascalau, Nicoleta ^{[1
]}

Marcu, Florin ^{[1
]}

机构：

[1] Univ Oradea, Fac Med & Pharm, Dept Psychoneurosciences & Rehabil, Oradea 410073, Romania

[2] Univ Oradea, Fac Med & Pharm, Dept Preclin Sci, Oradea 410073, Romania

[3] Univ Oradea, Fac Med & Pharm, Oradea 410073, Romania

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2023年 / 24卷 / 03期

关键词：

neuroinflammation; inflammaging; Alzheimer's disease; microglia; cellular senescence; TNF signaling; TREM2; oxidative stress; therapy; MILD COGNITIVE IMPAIRMENT; REGULATORY T-CELLS; AMYLOID-BETA; A-BETA; MITOCHONDRIAL FISSION; OXIDATIVE STRESS; ENDOPLASMIC-RETICULUM; CEREBROSPINAL-FLUID; MICROGLIAL ACTIVATION; INTERFERON EXPRESSION;

D O I：

10.3390/ijms24031869

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aging is the most prominent risk factor for late-onset Alzheimer's disease. Aging associates with a chronic inflammatory state both in the periphery and in the central nervous system, the evidence thereof and the mechanisms leading to chronic neuroinflammation being discussed. Nonetheless, neuroinflammation is significantly enhanced by the accumulation of amyloid beta and accelerates the progression of Alzheimer's disease through various pathways discussed in the present review. Decades of clinical trials targeting the 2 abnormal proteins in Alzheimer's disease, amyloid beta and tau, led to many failures. As such, targeting neuroinflammation via different strategies could prove a valuable therapeutic strategy, although much research is still needed to identify the appropriate time window. Active research focusing on identifying early biomarkers could help translating these novel strategies from bench to bedside.

引用

页数：46

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