Publications by authors named "Bruno Herculano"

Article Synopsis
  • Multiple sclerosis (MS) is an inflammatory central nervous system disease marked by myelin loss and neuronal issues, with most cases being non-familial but some familial forms identified.
  • Researchers conducted whole-exome sequencing on 132 patients from 34 multi-incident families, identifying likely pathogenic variants in 12 genes related to the innate immune system, which influence inflammation.
  • The identified variants point to a disruption in key immune and inflammatory pathways, providing insight into the chronic inflammation, demyelination, and neurodegeneration associated with familial MS.
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Down Syndrome (DS) patients develop characteristic Alzheimer's Disease (AD) neuropathology after their middle age. Prominent neuronal loss has been observed in the cortical regions of AD brains. However, the underlying mechanism leading to this neuronal loss in both DS and AD remains to be elucidated.

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Article Synopsis
  • Oxygen-glucose deprivation (OGD) in brain cells increases glutamate levels, leading to excitotoxicity due to decreased uptake by transporters affected by oxidative stress.
  • Atorvastatin, a cholesterol-lowering drug, shows potential neuroprotective effects by enhancing cell viability in brain slices following OGD and reoxygenation, likely by reducing oxidative stress.
  • The protective effects of atorvastatin involve improving glutamate uptake and glutamine synthetase activity, and its efficacy depends on its ability to inhibit cholesterol synthesis.
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  • The study explores how modulation of glutamate transmission can offer neuroprotection against excitotoxicity in neurodegenerative diseases and acute brain events.
  • It evaluates the effects of NMDA preconditioning on behavioral and EEG responses in mice, specifically focusing on spike-wave discharges and seizure behaviors after administering quinolinic acid.
  • Findings indicate that NMDA preconditioning increases spike-wave activity but protects against behavioral seizures from subsequent QA exposure, suggesting a potential therapeutic pathway for reducing seizure severity.
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Our goal in this study was to determine whether or not feeding young (4 months old) Alzheimer's disease model transgenic mice with a high fat diet (HFD), consisting of 32% fat, is capable of causing cognitive decline and whether treatment with β-alanyl-L-histidine (carnosine) is capable of reducing these effects. Carnosine is an endogenous antioxidant and antiglycating agent that is abundantly present in the brain and muscle tissues of vertebrates. After 8 weeks of feeding with HFD, we observed a significant decline in the contextual memory in transgenic mice fed with HFD as compared to transgenic mice fed with a normal diet as well as to normal diet-wild type mice.

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In this study, diffusion tensor MRI was used to examine the restoration of the cerebral white matter of macaque monkeys after unilateral cerebral multiple microinfarctions. Post-stroke, the monkeys showed deficits in several neurological functions, including motor functions, but most of the deficits resolved within 6 weeks. Very interestingly, the fractional anisotropy (a value determined by diffusion tensor MRI), of the monkeys' affected motor pathways dropped transiently, indicating a damage in the neural tracts.

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Traumatic brain injury (TBI) causes impairment of fine motor functions in humans and nonhuman mammals that often persists for months after the injury occurs. Neuroprotective strategies for prevention of the sequelae of TBI and understanding the molecular mechanisms and cellular pathways are related to the glutamatergic system. It has been suggested that cellular damage subsequent to TBI is mediated by the excitatory neurotransmitters, glutamate and aspartate, through the excessive activation of the N-methyl-D-aspartate (NMDA) receptors.

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