Publications by authors named "C Chillotti"

Article Synopsis
  • Mitochondrial dysfunction has been noted in bipolar disorder (BD), but its impact on the disorder's origins and treatment response remains under-researched.* -
  • A study comparing mitochondrial DNA copy number (mtDNA-cn) in 89 BD patients and 78 healthy controls found that BD patients had significantly higher mtDNA-cn levels, especially those treated with other mood stabilizers as opposed to lithium.* -
  • The results indicate that while BD may be linked to mitochondrial issues, lithium treatment appears to lower mtDNA-cn levels, suggesting a potential restoration of mitochondrial function that doesn't necessarily correlate with how well patients respond to the medication.*
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High rates of metabolic risk factors contribute to premature mortality in patients with severe mental disorders, but the molecular underpinnings of this association are largely unknown. We performed the first analysis on shared genetic factors between severe mental disorders and metabolic traits considering the effect of sex. We applied an integrated analytical pipeline on the largest sex-stratified genome-wide association datasets available for bipolar disorder (BD), major depressive disorder (MDD), schizophrenia (SZ), and for body mass index (BMI) and waist-to-hip ratio (WHR) (all including participants of European origin).

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Introduction: Discriminating bipolar disorder (BD) from major depressive disorder (MDD) remains a challenging clinical task. Identifying specific peripheral biosignatures that can differentiate between BD and MDD would significantly increase diagnostic accuracy. Dysregulated neuroplasticity is implicated in BD and MDD, and psychotropic medications restore specific disrupted processes by increasing neurotrophic signalling.

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Patients with severe mental disorders such as bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD) show a substantial reduction in life expectancy, increased incidence of comorbid medical conditions commonly observed with advanced age and alterations of aging hallmarks. While severe mental disorders are heritable, the extent to which genetic predisposition might contribute to accelerated cellular aging is not known. We used bivariate causal mixture models to quantify the trait-specific and shared architecture of mental disorders and 2 aging hallmarks (leukocyte telomere length [LTL] and mitochondrial DNA copy number), and the conjunctional false discovery rate method to detect shared genetic loci.

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