A Case Series of Patients With Polyneuropathy Due to Copper Deficiency.

We are presenting six cases of patients with peripheral polyneuropathy due to malnutrition in settings of prior history of gastric bypass surgery, zinc-based dentures usage, or long-standing alcohol abuse. The clinical presentation in all six patients included sensory, motor, or combined peripheral polyneuropathy and gait instability due to imbalance. All patients included in this case series were found to have low copper levels. Electromyography (EMG) with nerve conduction study (NCS) showed predominantly axonal and length dependent sensory or sensory-motor polyneuropathies. Patients were treated with copper supplements with reportable improvement in their presenting symptoms.

The "Medicare effect" on head and neck cancer diagnosis and survival.

BACKGROUND: Uninsured individuals age 55-64 experience disproportionately poor outcomes compared to their insured counterparts. Adequate coverage may prevent these delays. This study investigates a "Medicare-effect" on head and neck squamous cell carcinoma (HNSCC) diagnosis and treatment. METHODS: The Surveillance, Epidemiology, and End Results (SEER) database was queried for persons ages 60-70 years in the United States from 2000 to 2016 with HNSCC. A "Medicare effect" was defined as an increase in incidence, reduction in advanced stage presentation, and/or decrease in cancer-specific mortality (CSM). RESULTS: Compared to their Medicaid or uninsured counterparts, patients age 65 have an increased incidence of HNSCC diagnosis, reduction in advanced stage presentation, decrease in cancer-specific mortality, and higher likelihood of receiving cancer-specific surgery. CONCLUSIONS: Patients age 65 with Medicare have decreased incidence of HNSCC, less hazard of late-stage diagnosis, and lower cancer-specific mortality than their Medicaid or uninsured counterparts, supporting the idea of a "Medicare effect" in HNSCC.

Adropin correlates with aging-related neuropathology in humans and improves cognitive function in aging mice.

The neural functions of adropin, a secreted peptide highly expressed in the brain, have not been investigated. In humans, adropin is highly expressed in astrocytes and peaks during critical postnatal periods of brain development. Gene enrichment analysis of transcripts correlating with adropin expression suggests processes relevant to aging-related neurodegenerative diseases that vary with age and dementia state, possibly indicating survivor bias. In people aged <40 y and 'old-old' (>75 y) diagnosed with dementia, adropin correlates positively with genes involved in mitochondrial processes. In the 'old-old' without dementia adropin expression correlates positively with morphogenesis and synapse function. Potent neurotrophic responses in primary cultured neurons are consistent with adropin supporting the development and function of neural networks. Adropin expression in the 'old-old' also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in those without dementia. How variation in brain adropin expression affects neurological aging was investigated using old (18-month) C57BL/6J mice. In mice adropin is expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia and shows correlative relationships with groups of genes involved in neurodegeneration and cellular metabolism. Increasing adropin expression using transgenesis improved spatial learning and memory, novel object recognition, resilience to exposure to new environments, and reduced mRNA markers of inflammation in old mice. Treatment with synthetic adropin peptide also reversed age-related declines in cognitive functions and affected expression of genes involved in morphogenesis and cellular metabolism. Collectively, these results establish a link between adropin expression and neural energy metabolism and indicate a potential therapy against neurological aging.