Publications by authors named "Danielle Herman"
Article Synopsis
- Spinal cord ischemia (SCI) is a rare but serious complication that can occur after thoracic endovascular aortic repair (TEVAR), mainly due to reduced blood supply to the spinal cord.
- A case study of a 67-year-old patient showed that delayed SCI occurred nearly two years post-TEVAR, presenting as acute paraplegia triggered by pre-syncope and a thrombosed endoleak, along with the patient's existing vascular issues.
- Treatment strategies, including CSF drainage and MAP augmentation, led to moderate recovery, emphasizing the importance of quick diagnosis and intervention to prevent worsening of spinal cord injury after TEVAR.
Metabolic syndrome (MetS), characterized by hyperglycemia, obesity, and hyperlipidemia, can increase the risk of developing late-onset dementia. Recent studies in patients and mouse models suggest a putative link between hyperphosphorylated tau, a component of Alzheimer's disease-related dementia (ADRD) pathology, and cerebral glucose hypometabolism. Impaired glucose metabolism reduces glucose flux through the hexosamine metabolic pathway triggering attenuated O-linked N-acetylglucosamine (O-GlcNAc) protein modification.
View Article and Find Full Text PDFBackground: Detecting cortical demyelination using magnetic resonance imaging (MRI) in multiple sclerosis (MS) remains a challenge. Magnetization transfer ratio (MTR), T1-weighted/T2-weighted ratio (T1T2R), and T2-weighted (T2w) signal are sensitive to cortical demyelination, but their accuracy is unknown.
Objectives: To quantify the sensitivity, specificity, and accuracy of postmortem T1T2R, MTR, and T2w in detecting cortical demyelination.
Objective: Describe magnetic resonance imaging (MRI) susceptibility changes in progressive multifocal leukoencephalopathy (PML) and identify neuropathological correlates.
Methods: PML cases and matched controls with primary central nervous system lymphoma (PCNSL) were retrospectively identified. MRI brain at 3 T and 7 T were reviewed.
Developmental exposure to the organochlorine pesticide dieldrin causes male-specific exacerbation of α-synuclein-preformed fibril-induced toxicity and motor deficits.
Neurobiol Dis
July 2020
Article Synopsis
- Exposure to the pesticide dieldrin is linked to a higher risk of Parkinson's disease (PD), and previous studies indicated that it makes neurons more sensitive to toxic substances like MPTP in mice.
- This study used a new model involving α-synuclein pre-formed fibrils (PFFs) to see if dieldrin exposure during development raises vulnerability to PD-like conditions.
- Results showed that male mice exposed to dieldrin had worsened motor skills and increased dopamine turnover after PFF exposure, but didn't show increased aggregation of α-synuclein or loss of certain neurons, highlighting a male-specific response to dieldrin's effects on neurotoxicity.