Environmental enrichment reverses cognitive impairments and hippocampus tissue loss without altering the redox state in rats exposed to severe chronic hyperhomocysteinemia.

Introduction: Classical homocystinuria is a genetic disease caused by partial or total deficiency of cystathionine-β synthase (CβS) enzyme activity, ultimately leading to brain alterations and early atherosclerotic disease. Currently, there is no cure for the disease and the treatments consist in reducing homocysteine levels through diet, however not all patients respond to therapy. Due to its ability to increase neurotrophins production and decrease oxidative stress in the brain, environmental enrichment (EE) has been used with success as an adjuvant non-pharmacological therapy for CNS disorders.

Maternal lactoferrin supplementation prevents mitochondrial and redox homeostasis dysfunction, and improves antioxidant defenses through Nrf2 and UCP2 signaling after neonatal hypoxia-ischemia.

Neonatal hypoxia-ischemia (HI) is a major cause of mortality and neurological impairments in infants. Main HI-induced pathological mechanisms include mitochondrial dysfunction and oxidative stress due to insufficient oxygen and energetic substrates to the nervous cells. Bovine lactoferrin (Lf) has demonstrated neuroprotective effects in several experimental models of neonatal brain injury in rodents, however its mechanisms remain unclear.

Use of mechanical insufflation-exsufflation devices among intensive care units in Brazil.

Despite its potential benefits, it is unclear how professionals use mechanical insufflation-exsufflation (MI-E) in Brazilian intensive care units (ICUs). This survey aimed to describe MI-E use among health care professionals registered with the Brazilian Association of Intensive Care. Cross-sectional electronic survey of health care professionals (physicians, physiotherapists and nurses) registered with the Brazilian Association of Intensive Care.

Sex-specific cognitive benefits and anti-inflammatory effects of coumestrol pretreatment in transient global cerebral ischemia.

Cerebral Global Ischemia (CGI) is a devastating neurological condition affecting millions globally each year, leading to significant inflammatory responses and long-term consequences, including delayed neuronal death and neurocognitive impairment. Following brain injury, resident microglial cells are activated, triggering pro-inflammatory cytokine expression and altering neuroimmune processes in a sex-dependent manner, particularly within the hippocampus. Coumestrol, a plant estrogen, is promoted as an alternative to post-menopausal hormone therapy due to its various mechanisms that enhance brain health, including its anti-inflammatory effects.

α-Ketoisocaproic Acid Disrupts Mitochondrial Bioenergetics in the Brain of Neonate Rats: Molecular Modeling Studies of α-ketoglutarate Dehydrogenase Subunits Inhibition.

Brain accumulation of the branched-chain α-keto acids α-ketoisocaproic acid (KIC), α-keto-β-methylvaleric acid (KMV), and α-ketoisovaleric acid (KIV) occurs in maple syrup urine disease (MSUD), an inherited intoxicating metabolic disorder caused by defects of the branched-chain α-keto acid dehydrogenase complex. Patients commonly suffer life-threatening acute encephalopathy in the newborn period and develop chronic neurological sequelae of still undefined pathogenesis. Therefore, this work investigated the in vitro influence of pathological concentrations of KIC (5 mM), KMV (1 mM), and KIV (1 mM) on mitochondrial bioenergetics in the cerebral cortex of neonate (one-day-old) rats.