Hippocampal Nogo66‐NgR1 signaling activation restricts postsynaptic assembly in aged mice with postoperative neurocognitive disorders DOI Creative Commons
Min Jia,

G Li,

Chen Jiang

и другие.

Aging Cell, Год журнала: 2024, Номер unknown

Опубликована: Окт. 16, 2024

Abstract Postoperative neurocognitive disorders (pNCD) are a common neurological complication, especially in elderly following anesthesia and surgery. Yet, the underlying mechanisms of pNCD remain elusive. This study aimed to investigate molecular that compromise synaptic metaplasticity development with focus on involvement Nogo‐66 receptor 1 (NgR1) pathogenesis aged mice. Aged mice subjected laparotomy surgery exhibited anxiety‐like behavior contextual fear memory impairment. Moreover, procedure significantly increased NogoA NgR1 expressions, particularly hippocampal CA1 CA3 regions. increase led depolymerization F‐actin, attributed activation RhoA‐GTPase, resulting reduction dendritic spines changes their morphology. Additionally, these hindered efficient postsynaptic delivery subunit GluA1 GluA2 AMPA receptors (AMPARs), consequently diminishing excitatory neurotransmission hippocampus. Importantly, administering competitive antagonist peptide NEP1‐40 (Nogo‐A extracellular residues 1–40 amino acids Nogo‐66) Fasudil (a Rho‐kinase inhibitor) effectively mitigated impairments reversed deficits Our work indicates high Nogo66‐NgR1 signaling disrupts surface due F‐actin pathophysiology pNCD.

Язык: Английский

Mitophagy-associated programmed neuronal death and neuroinflammation DOI Creative Commons

Yanlin Zhu,

Jianning Zhang,

Quanjun Deng

и другие.

Frontiers in Immunology, Год журнала: 2024, Номер 15

Опубликована: Окт. 2, 2024

Mitochondria are crucial organelles that play a central role in cellular metabolism and programmed cell death eukaryotic cells. Mitochondrial autophagy (mitophagy) is selective process where damaged mitochondria encapsulated degraded through autophagic mechanisms, ensuring the maintenance of both mitochondrial homeostasis. Excessive neurons can result functional impairments following cerebral ischemia trauma, as well chronic neurodegenerative diseases, leading to irreversible declines motor cognitive functions. Neuroinflammation, an inflammatory response nervous system factors disrupting homeostasis, common feature across various neurological events, including ischemic, infectious, traumatic, conditions. Emerging research suggests regulating may offer promising therapeutic avenue for treating certain diseases. Furthermore, existing literature indicates small molecule regulators have been tested animal models linked disease outcomes. This review explores mitophagy neuronal its connection neuroinflammation.

Язык: Английский

Процитировано

1
Hippocampal Nogo66‐NgR1 signaling activation restricts postsynaptic assembly in aged mice with postoperative neurocognitive disorders DOI Creative Commons
Min Jia,

G Li,

Chen Jiang

и другие.

Aging Cell, Год журнала: 2024, Номер unknown

Опубликована: Окт. 16, 2024

Abstract Postoperative neurocognitive disorders (pNCD) are a common neurological complication, especially in elderly following anesthesia and surgery. Yet, the underlying mechanisms of pNCD remain elusive. This study aimed to investigate molecular that compromise synaptic metaplasticity development with focus on involvement Nogo‐66 receptor 1 (NgR1) pathogenesis aged mice. Aged mice subjected laparotomy surgery exhibited anxiety‐like behavior contextual fear memory impairment. Moreover, procedure significantly increased NogoA NgR1 expressions, particularly hippocampal CA1 CA3 regions. increase led depolymerization F‐actin, attributed activation RhoA‐GTPase, resulting reduction dendritic spines changes their morphology. Additionally, these hindered efficient postsynaptic delivery subunit GluA1 GluA2 AMPA receptors (AMPARs), consequently diminishing excitatory neurotransmission hippocampus. Importantly, administering competitive antagonist peptide NEP1‐40 (Nogo‐A extracellular residues 1–40 amino acids Nogo‐66) Fasudil (a Rho‐kinase inhibitor) effectively mitigated impairments reversed deficits Our work indicates high Nogo66‐NgR1 signaling disrupts surface due F‐actin pathophysiology pNCD.

Язык: Английский

Процитировано

1