Publications by authors named "Colby L Samstag"
Introduction: We investigated whether the cerebellum develops neuropathology that correlates with well-accepted Alzheimer's disease (AD) neuropathological markers and cognitive status.
Methods: We studied cerebellar cytoarchitecture in a cohort (N = 30) of brain donors. In a larger cohort (N = 605), we queried whether the weight of the contents of the posterior fossa (PF), which contains primarily cerebellum, correlated with dementia status.
Article Synopsis
- The cerebellum is crucial for motor, cognitive, and emotional functions; its decline in aging has led to increased scientific interest due to its role in timing and complex tasks like spatial navigation.
- Anatomical connections and interactions with the basal ganglia, cerebral cortex, and spinal cord suggest that the cerebellum creates internal models that aid in automatic behaviors; changes in its structure and function with age are linked to mobility and cognitive decline.
- Neuroimaging studies indicate that age-related cerebellar atrophy correlates with cognitive and motor performance issues, and in conditions like Alzheimer's, cerebellar function declines independently from the cerebral cortex's contributions.
Article Synopsis
- Somatic mutations in mitochondrial DNA (mtDNA) are associated with diseases and aging, and a new model using a cytidine deaminase, APOBEC1, induces specific mutations in Drosophila.
- Unlike previous models that led to a high quantity of mutations with minimal effects on lifespan, mito-APOBEC1 induces only C:G>T:A transitions which significantly disrupts mitochondrial function.
- The study highlights that the type of mutations (quality) is more important than the number of mutations (quantity) in affecting the overall fitness and health of the organism.
Mitochondrial DNA (mtDNA) mutations cause severe maternally inherited syndromes and the accumulation of somatic mtDNA mutations is implicated in aging and common diseases. However, the mechanisms that influence the frequency and pathogenicity of mtDNA mutations are poorly understood. To address this matter, we created a Drosophila mtDNA mutator strain expressing a proofreading-deficient form of the mitochondrial DNA polymerase.
View Article and Find Full Text PDFGrowing evidence implicates neurons that project from the lateral parabrachial nucleus (LPBN) to the hypothalamic ventromedial nucleus (VMN) in a neurocircuit that drives counterregulatory responses to hypoglycemia, including increased glucagon secretion. Among LPBN neurons in this circuit is a subset that expresses cholecystokinin (LPBNCCK neurons) and is tonically inhibited by leptin. Because uncontrolled diabetes is associated with both leptin deficiency and hyperglucagonemia, and because intracerebroventricular (ICV) leptin administration reverses both hyperglycemia and hyperglucagonemia in this setting, we hypothesized that deficient leptin inhibition of LPBNCCK neurons drives activation of this LPBN→VMN circuit and thereby results in hyperglucagonemia.
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