The role of glial autophagy in Alzheimer's disease

被引:22
|
作者
Litwiniuk, Anna [1 ]
Juszczak, Grzegorz Roman [2 ]
Stankiewicz, Adrian Mateusz [3 ]
Urbanska, Kaja [4 ]
机构
[1] Ctr Postgrad Med Educ, Dept Neuroendocrinol, Warsaw, Mazovia, Poland
[2] Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Anim Behav & Welf, Jastrzebiec, Mazovia, Poland
[3] Polish Acad Sci, Inst Genet & Anim Biotechnol, Dept Mol Biol, Jastrzebiec, Mazovia, Poland
[4] Warsaw Univ Life Sci, Dept Morphol Sci, Fac Vet Med, Warsaw, Mazovia, Poland
关键词
OLIGODENDROCYTE PRECURSOR CELLS; AMYOTROPHIC-LATERAL-SCLEROSIS; ALPHA-SYNUCLEIN; MOUSE MODEL; OXIDATIVE STRESS; MICROGLIAL ACTIVATION; REACTIVE ASTROCYTES; IMPAIRED AUTOPHAGY; BETA ACCUMULATION; PATHOLOGY;
D O I
10.1038/s41380-023-02242-5
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
Although Alzheimer's disease is the most pervasive neurodegenerative disorder, the mechanism underlying its development is still not precisely understood. Available data indicate that pathophysiology of this disease may involve impaired autophagy in glial cells. The dysfunction is manifested as reduced ability of astrocytes and microglia to clear abnormal protein aggregates. Consequently, excessive accumulation of amyloid beta plaques and neurofibrillary tangles activates microglia and astrocytes leading to decreased number of mature myelinated oligodendrocytes and death of neurons. These pathologic effects of autophagy dysfunction can be rescued by pharmacological activation of autophagy. Therefore, a deeper understanding of the molecular mechanisms involved in autophagy dysfunction in glial cells in Alzheimer's disease may lead to the development of new therapeutic strategies. However, such strategies need to take into consideration differences in regulation of autophagy in different types of neuroglia.
引用
收藏
页码:4528 / 4539
页数:12
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