Human aging is characterized by low-grade, chronic, systemic inflammation in aging, in the absence of overt infection and is a highly significant risk factor for both morbidity and mortality in the elderly people [ 2 ].
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Age-related cognitive impairment is associated with long-term neuroinflammation and oxidative stress in a mouse model of episodic systemic inflammation.
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Total number of microglia skeleton segments was lower in the aged mice (young 415 ± 57 vs aged 118 ± 13, p < 0.0001) whereas young SI showed a trend towards a diminution of microglial cell ramification number (Fig. 3 c).