Publications by authors named "T Deierborg"

Article Synopsis
  • Parkinson's Disease (PD) is linked to the loss of dopamine-producing neurons, with apoptosis being a significant factor in its progression.
  • A study created a genetic model (TH-C3KO) to investigate the effects of removing the apoptosis-related gene Casp3 in dopaminergic neurons, finding that this deletion did not provide long-term protection against neuron loss and actually switched the cell death mechanism to necrosis.
  • The research also revealed an intensified microglial response in TH-C3KO mice, indicating that targeting galectin-3 and microglial behavior could be more effective strategies for developing PD therapies instead of focusing solely on apoptosis inhibition.
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Dietary patterns that include an excess of foods rich in saturated fat are associated with brain dysfunction. Although microgliosis has been proposed to play a key role in the development of brain dysfunction in diet-induced obesity (DIO), neuroinflammation with cytokine over-expression is not always observed. Thus, mechanisms by which microglia contribute to brain impairment in DIO are uncertain.

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Galectin-3 (Gal-3) is a multifunctional protein that plays a pivotal role in the initiation and progression of various central nervous system diseases, including cancer. Although the involvement of Gal-3 in tumour progression, resistance to treatment and immunosuppression has long been studied in different cancer types, mainly outside the central nervous system, its elevated expression in myeloid and glial cells underscores its profound impact on the brain's immune response. In this context, microglia and infiltrating macrophages, the predominant non-cancerous cells within the tumour microenvironment, play critical roles in establishing an immunosuppressive milieu in diverse brain tumours.

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Aims: According to Braak's hypothesis, it is plausible that Parkinson's disease (PD) originates in the enteric nervous system (ENS) and spreads to the brain through the vagus nerve. In this work, we studied whether inflammatory bowel diseases (IBDs) in humans can progress with the emergence of pathogenic α-synuclein (α-syn) in the gastrointestinal tract and midbrain dopaminergic neurons.

Methods: We have analysed the gut and the ventral midbrain from subjects previously diagnosed with IBD and form a DSS-based rat model of gut inflammation in terms of α-syn pathology.

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