C. elegans is a powerful model for analysis of the conserved mechanisms that modulate healthy aging. In the aging nematode nervous system, neuronal death and/or detectable loss of processes are not readily apparent, but because dendrite restructuring and loss of synaptic integrity are hypothesized to contribute to human brain decline and dysfunction, we combined fluorescence microscopy and electron microscopy (EM) to screen at high resolution for nervous system changes. We report two major components of morphological change in the aging C. elegans nervous system: 1) accumulation of novel outgrowths from specific neurons, and 2) physical decline in synaptic integrity. Novel outgrowth phenotypes, including branching from the main dendrite or new growth from somata, appear at a high frequency in some aging neurons, but not all. Mitochondria are often associated with age-associated branch sites. Lowered insulin signaling confers some maintenance of ALM and PLM neuron structural integrity into old age, and both DAF-16/FOXO and heat shock factor transcription factor HSF-1 exert neuroprotective functions. hsf-1 can act cell autonomously in this capacity. EM evaluation in synapse-rich regions reveals a striking decline in synaptic vesicle numbers and a dimunition of presynaptic density size. Interestingly, old animals that maintain locomotory prowess exhibit less synaptic decline than same-age decrepit animals, suggesting that synaptic integrity correlates with locomotory healthspan. Our data reveal similarities between the aging C. elegans nervous system and mammalian brain, suggesting conserved neuronal responses to age. Dissection of neuronal aging mechanisms in C. elegans may thus influence the development of brain healthspan-extending therapies.

The protein level in the cerebrospinal fluid (CSF) is an important diagnostic tool and, when abnormal, can provide clinicians with clues to the etiology of a patient's condition. Froin's syndrome has been described in previous literature as the combination of xanthochromia, elevated protein, and hypercoagulated CSF. The pathophysiology behind Froin's syndrome is thought to be due to stagnant CSF causing passive and/or active diffusive processes, resulting in hyperproteinosis and hypercoagulation. We present a case of Froin's syndrome in a patient with cervical spine trauma whose extraordinary level of CSF proteinosis helped raise suspicion for underlying obstructive and infectious etiology.

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Traumatic brain injury (TBI) is among the most common causes of death in trauma patients. The exact etiology of mortality is poorly understood. Catecholamine surges seen in these patients are known to prompt arrhythmogenesis. We attempted to better characterize the correlation between traumatic brain injury and arrhythmogenesis. METHODS: A composite database of National Inpatient Sample (NIS) for 2016 and 2017 was queried using ICD-10 codes to identify patients with dysrhythmia among a cohort of patients with traumatic brain injury. A propensity weighted logistic regression analysis was performed controlling for age, gender, and comorbidities. Propensity weighted cohorts were compared for correlation with dysrhythmia by age category.

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