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2017 ; 8
(ä): 65
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English Wikipedia
Parkinson s disease: Microglial/macrophage-induced immunoexcitotoxicity as a
central mechanism of neurodegeneration
#MMPMID28540131
Blaylock RL
Surg Neurol Int
2017[]; 8
(ä): 65
PMID28540131
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Parkinson's disease is one of the several neurodegenerative disorders that
affects aging individuals, with approximately 1% of those over the age of 60
years developing the disorder in their lifetime. The disease has the
characteristics of a progressive disorder in most people, with a common pattern
of pathological change occurring in the nervous system that extends beyond the
classical striatal degeneration of dopaminergic neurons. Earlier studies
concluded that the disease was a disorder of alpha-synuclein, with the formation
of aggregates of abnormal alpha-synuclein being characteristic. More recent
studies have concluded that inflammation plays a central role in the disorder and
that the characteristic findings can be accounted for by either mutation or
oxidative damage to alpha-synuclein, with resulting immune reactions from
surrounding microglia, astrocytes, and macrophages. What has been all but ignored
in most of these studies is the role played by excitotoxicity and that the two
processes are intimately linked, with inflammation triggered cell signaling
enhancing the excitotoxic cascade. Further, there is growing evidence that it is
the excitotoxic reactions that actually cause the neurodegeneration. I have
coined the name immunoexcitotoxicity to describe this link between inflammation
and excitotoxicity. It appears that the two processes are rarely, if ever,
separated in neurodegenerative diseases.