=====Caspase-1=====
Observations of the interactions between the inflammatory cytokine interleuldn-1 (IL-1) beta and the inflammatory/apoptotic caspase-1 and their involvement in age-related impairments in cognition. A comprehensive understanding of these mechanisms could potentially lead to the development of preventive or protective therapies that reduce or inhibit the cognitive decline associated with aging and age-related neurodegenerative disease
((Gemma C, Bickford PC. Interleukin-1beta and caspase-1: players in the
regulation of age-related cognitive dysfunction. Rev Neurosci. 2007;18(2):137-48.
Review. PubMed PMID: 17593876.
)).

Blockade of caspase-1 increases neurogenesis in the aged hippocampus
((Gemma C, Bachstetter AD, Cole MJ, Fister M, Hudson C, Bickford PC. Blockade of
caspase-1 increases neurogenesis in the aged hippocampus. Eur J Neurosci. 2007
Nov;26(10):2795-803. PubMed PMID: 18001276.)).

The [[caspase]] 1 T activation complexes ([[inflammasome]]s) can facilitate caspase-1 and IL-1β processing, which amplifies the inflammatory response. In a study Li et al. examined whether caspase-1 activation contributes to irradiation-induced damage to neural stem and progenitor cells (NSPCs). They found that X-ray irradiation induced activation of caspase-1 in NSPCs in vitro and in vivo. Next, using a caspase-1 inhibitor ([[Ac-YVAD-CMK]]) to block caspase-1 activation in vitro and in vivo, we further demonstrated that X-ray irradiation may inhibit proliferation, induce senescence of NSPCs through caspase-1 activation. Together, these results suggest that caspase-1 activation is involved in irradiation-induced damage to NSPCs
((Li T, Li L, Li F, Liu Y. X-ray irradiation accelerates senescence in
hippocampal neural stem/progenitor cells via caspase-1 activation. Neurosci Lett.
2015 Jan 12;585:60-5. doi: 10.1016/j.neulet.2014.11.028. Epub 2014 Nov 20. PubMed
PMID: 25445379.))
----
Rashad et al., from  [[Sendai]], [[Japan]] showed the intense activation of [[immune cell]]s, particularly the [[microglia]], along with the increase in [[macrophage]] activity and [[NLRP3]] [[inflammasome]] activation that is indicated by NLRP3, [[Interleukin 1 beta]] (IL-1β), and [[Interleukin 18]] gene and [[caspase 1]] [[upregulation]] and [[cleavage]] as well as [[pyroptosis]].

[[Leukocyte]]s were observed in the brain [[parenchyma]], indicating a role in [[cerebral venous thrombosis]] (CVT)-induced [[inflammation]]. In addition, [[astrocyte]]s were activated, and they induced [[glial scar]] leading to parenchymal contraction during the [[subacute]] stage and [[tissue]] loss. [[MMP9]] was responsible primarily for the [[BBB]] breakdown after CVT and it is mainly produced by [[pericyte]]s. MMP9 activation was observed before inflammatory changes, indicating that BBB breakdown is the initial driver of the pathology of CVT. These results show an inflammation driven pathophysiology of CVT that follows MMP9-mediated BBB breakdown, and identified several targets that can be targeted by pharmaceutical agents to improve the [[neuroinflammation]] that follows CVT, such as MMP9, NLRP3, and IL-1β. Some of these pharmaceutical agents are already in clinical practice or under clinical trials indicating a good potential for translating this work into patient care
((Rashad S, Niizuma K, Sato-Maeda M, Fujimura M, Mansour A, Endo H, Ikawa S,
Tominaga T. Early BBB breakdown and subacute inflammasome activation and
pyroptosis as a result of cerebral venous thrombosis. Brain Res. 2018 Jul 4. pii:
S0006-8993(18)30362-7. doi: 10.1016/j.brainres.2018.06.029. [Epub ahead of print]
PubMed PMID: 29981290.
)).