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Daniel Rob
Daniel Rob

Activation Inventor Professional 2019 Activation

indeed, it is well known that activated microglia and astrocytes with excessive cytokine secretion (such as tnf-α, il-1, il-6, and il-8) can lead to progressive neuronal death, in both acute and chronic neurodegenerative diseases (10, 11). more recently, it has been suggested that microglial and astroglial cells not only contribute to the neuroinflammatory response but also modulate the survival of neurons in the vicinity of activated microglia or astrocytes (12). in addition, current evidence suggests that dysregulated astroglial and microglial cells can produce excessive amounts of molecules (e.g., aβ) and neurotransmitters (e., glutamate) that are associated with the development and progression of ad (13). furthermore, although not necessarily linked with microglial activation, astrocytes can affect the development of aβ pathology in the ad brain through the release of several molecules, such as nitric oxide (no), atp, prostaglandin e2 (pge2), serotonin (5-ht) (14).

Activation Inventor Professional 2019 Activation

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thus, in the present study, we investigated the levels of soluble trem2 in the csf to evaluate the early microglial activation phase [ 65 ] and ykl-40 and cx3cl1 as markers for astroglial activation [ 66 ] in ad patients. importantly, the elevated levels of these three markers were found to correlate with the severity of cognitive impairment, supporting the involvement of the innate immune system in the pathogenesis of ad. of note, none of the ad patients showed any clinical signs of an infectious disease or any other systemic inflammatory disease in our previous study [ 65 ].

the present results may have important implications for the understanding of the evolution of ad pathophysiology and for the development of new therapeutic approaches for ad. by defining the stage of disease during which the immune response is in balance or dysregulated, it may be possible to define patients that are more responsive to therapies that aim to restore the immune balance. in particular, it may be possible to identify patients with ad who have not yet begun to show cognitive decline. we will investigate the role of immune activation in ad in subsequent studies.




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