Retinal Ganglion Cell Subtypes and Their Vulnerability in Glaucoma.

The detection of selective retinal ganglion cell damage in glaucoma has been a long sought-after goal, not just for the development of clinical tests for the early detection of glaucoma but for the elucidation of potential mechanisms underlying retinal ganglion cell loss. Early reports of the selective vulnerability of larger retinal ganglion cells (RGCs) in human studies did not translate simply to the loss of a particular class of RGC but more likely reflected shrinkage and degeneration across all RGC classes. Subsequent studies of nonhuman primate (NHP) models of glaucoma indicated some selectivity with great damage to the magnocellular vs parvocellular pathways.

Oral nicotinamide provides robust, dose-dependent structural and metabolic neuroprotection of retinal ganglion cells in experimental glaucoma.

A compromised capacity to maintain NAD pools is recognized as a key underlying pathophysiological feature of neurodegenerative diseases. NAD acts as a substrate in major cell functions including mitochondrial homeostasis, cell signalling, axonal transport, axon/Wallerian degeneration, and neuronal energy supply. Dendritic degeneration is an early marker of neuronal stress and precedes cell loss.

Extracellular vesicle encapsulated nicotinamide delivered via a trans-scleral route provides retinal ganglion cell neuroprotection.

The progressive and irreversible degeneration of retinal ganglion cells (RGCs) and their axons is the major characteristic of glaucoma, a leading cause of irreversible blindness worldwide. Nicotinamide adenine dinucleotide (NAD) is a cofactor and metabolite of redox reaction critical for neuronal survival. Supplementation with nicotinamide (NAM), a precursor of NAD, can confer neuroprotective effects against glaucomatous damage caused by an age-related decline of NAD or mitochondrial dysfunction, reflecting the high metabolic activity of RGCs.

Gene Gun DiOlistic Labelling of Retinal Ganglion Cells.

Gene gun DiOlistic labelling enables the detailed visualization of retinal ganglion cells (RGCs) dendritic structure. Since the level of labelling is independent of cellular health, it is useful for the characterization of neuronal structure in degenerating neurons where expressed reporters may be inadequate. The method uses compressed helium gas to fire tungsten or gold microparticles coated in carbocyanine dyes (DiD, DiI, DiO) into flat mounted retinas.

Nicotinamide provides neuroprotection in glaucoma by protecting against mitochondrial and metabolic dysfunction.

Nicotinamide adenine dinucleotide (NAD) is a REDOX cofactor and metabolite essential for neuronal survival. Glaucoma is a common neurodegenerative disease in which neuronal levels of NAD decline. We assess the effects of nicotinamide (a precursor to NAD) on retinal ganglion cells (the affected neuron in glaucoma) in normal physiological conditions and across a range of glaucoma relevant insults including mitochondrial stress and axon degenerative insults.

Potential Therapeutic Benefit of NAD Supplementation for Glaucoma and Age-Related Macular Degeneration.

Glaucoma and age-related macular degeneration are leading causes of irreversible blindness worldwide with significant health and societal burdens. To date, no clinical cures are available and treatments target only the manageable symptoms and risk factors (but do not remediate the underlying pathology of the disease). Both diseases are neurodegenerative in their pathology of the retina and as such many of the events that trigger cell dysfunction, degeneration, and eventual loss are due to mitochondrial dysfunction, inflammation, and oxidative stress.

as a potential source of neuroactive compounds to promote and restore neural functions.

Nutraceuticals had always been known for their therapeutic effects in ancient medicine and had been the primary healing remedy until the introduction of modern chemistry and pharmacology. However, their use has not been dismissed but actually is acquiring a new acclamation among the scientific community especially for their efficacy on the Central Nervous System (CNS). Molecular mechanisms of the most common neurodegenerative diseases are now being uncovered and along with that the molecules that drive the neurodegenerative processes.

Work-related musculoskeletal disorders with reference to the revised occupational diseases list.

Due to the different compensation schemes, compensated musculoskeletal disorders vary widely between countries. In Italy, following the Constitutional Court Decision no.179/1988, these disorders were treated as "non-listed" diseases and workers must prove their occupational origin by submitting a compensation claim for musculoskeletal disorders to INAIL.

[Criteria for classification of upper limb work-related musculo-skeletal disorders due to biomechanical overload in occupational health. Consensus document by an Italian Working Group].

Background And Objective: In a preliminary consensus document the authors proposed criteria and methods to identify upper limb work-related MSDs due to biomechanical overload. With this document they intend to define severity according to shared models and procedures so as to fit behaviours to diagnostic procedures and their medical-legal assessment. This becomes especially important in view of Ministerial Decree of April 27 2004 fixing the new lists of diseases having a possible work-related origin that must be reported by law in accordance with art.