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.
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 is most abundant in neural tissues yet its neurological functions are unclear. Data from post-mortem human brain tissue samples indicates adropin expression occurs predominantly in astrocytes, peaks during critical post-natal periods of brain development, and then declines with aging. Previous experiments indicate adropin regulates mitochondrial metabolism. Gene clusters correlating with adropin are age- and dementia-specific, possibly indicating survivor bias. In people aged <40y adropin correlates positively with genes involved in mitochondrial metabolism, APOE and Clusterin. In the ‘old-old’ (>75y) with dementia, adropin expression correlates with genes linked to mitochondrial metabolism and neurodegenerative conditions. In the ‘old-old’ (>75y) without dementia, adropin correlates with genes involved in morphogenesis, growth of neuronal processes (dendrites, axons) and synapse function. Accordingly, adropin elicits neurotrophic responses in primary cultured neurons. Adropin expression also correlates positively with protein markers of tau-related neuropathologies and inflammation, particularly in people without dementia, indicating a link to cellular stressors. How variation in brain adropin expression affects neurological aging was investigated using C57BL/6J mice. In mice, adropin is more widely expressed in neurons, oligodendrocyte progenitor cells, oligodendrocytes, and microglia. Preventing the decline in expression observed with aging of mice using transgenesis improved cognitive function and resilience, while also reducing mRNA markers of inflammation in 18-month old mice. Treating 18-month old mice with adropin peptide also improved cognitive performance. These results link adropin expression to cellular energy metabolism and stress responses in the brain and indicates a possible relationship with aging-related cognitive decline.
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.
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