Ulcerated Necrobiosis Lipoidica.

A 23-year-old Caucasian female, with type I diabetes mellitus, presented with a 7-month history of two painful yellowish-red plaques with ulcerated centre in the left leg. A diagnosis of ulcerated necrobiosis lipoidica (NL) was made and she was started on pentoxifylline 400 mg tid and tacrolimus ointment 0.1%. After four months of treatment with no improvement, the patient was proposed for hyperbaric oxygen therapy (HBOT). Overall, she received a total of 30 sessions of HBOT, after which the wounds healed completely. There have been no recurrences in the 14 months following resolution.

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Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer’s mouse models

Abstract Nicotinamide adenine dinucleotide (NAD)(+), a coenzyme involved in redox activities in the mitochondrial electron transport chain, has been identified as a key regulator of the lifespan-extending effects, and the activation of NAD(+) expression has been...

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NAD+ biosynthesis, aging, and disease

Abstract Nicotinamide adenine dinucleotide (NAD+) biosynthesis and its regulation have recently been attracting markedly increasing interest. Aging is marked by a systemic decrease in NAD+ across multiple tissues. The dysfunction of NAD+ biosynthesis plays a critical...

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Hyperbaric oxygen therapy ameliorates pathophysiology of 3xTg-AD mouse model by attenuating neuroinflammation.

There is a real need for new interventions for Alzheimer’s disease (AD). Hyperbaric oxygen therapy (HBOT), the medical administration of 100% oxygen at conditions greater than 1 atmosphere absolute, has been used successfully to treat several neurological conditions, but its effects on AD pathology have never been thoroughly examined. Therefore, we exposed old triple-transgenic (3xTg) and non-transgenic mice to HBOT followed by behavioral, histological, and biochemical analyses. HBOT attenuated neuroinflammatory processes by reducing astrogliosis, microgliosis, and the secretion of proinflammatory cytokines (IL-1β and TNFα) and increasing expression of scavenger receptor A, arginase1, and antiinflammatory cytokines (IL-4 and IL-10). Moreover, HBOT reduced hypoxia, amyloid burden, and tau phosphorylation in 3xTg mice and ameliorated their behavioral deficits. Therefore, we suggest that HBOT has multifaceted effects that reduce AD pathologies, even in old mice. Given that HBOT is used in the clinic to treat various indications, including neurological conditions, these results suggest HBOT as a novel therapeutic intervention for AD.

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