Neurological Disorders and Glaucoma - An Overview
ABSTRACT Due to the anatomic location of the N. opticus to the brain and its embryological development as a "bulging part of the brain", a close connection between the opticoneuropathy and certain neurological diseases exists. Glaucoma is a chronic neurodegenerative disorder and many cellular and molecular mechanisms of the chronic neurodegenerative diseases are common in the brain. For example, elevated levels of multiple biomarkers of Alzheimer's disease were found in the aqueous humor of patients with primary open-angle glaucoma. Also a decreased cerebrospinal fluid pressure (CSFP) has been demonstrated in patients with glaucoma and Alzheimer's disease. The resulting translaminar pressure difference is seen as one of the pathogenic mechanisms of the formation of the optic neuropathy in both diseases. Other hypotheses, such as the influence of oxidative stress, excitotoxicity, mitochondrial dysfunction, genetic factors and vascular factors play additional roles in the pathogenesis of the different diseases. Experimental studies have shown that dopaminergic amacrine cells are present in the retina. The dopamine in the retina is necessary for the light adaptation and the signal processing in the rods and cones. Parkinson's disease is characterised by a loss of dopaminergic neurons in the basal ganglia-substantia nigra pars compacta of the midbrain. These decreased levels of dopamine also have an effect on the eye and the afferent signal processing. So there are reductions in visual acuity, disturbances in colour vision and contrast sensitivity and reduction of the retinal nerve fiber layer in patients affected with Parkinson's disease. With the examples of Alzheimer's disease, Parkinson's disease and the chronic inflammatory disease multiple sclerosis, we demonstrate the association between the neurological diseases and the opticoneuropathy in primary open-angle glaucoma.
SourceAvailable from: Ulrike Zimmermann[Show abstract] [Hide abstract]
ABSTRACT: The unconventional myosin VI, a member of the actin-based motor protein family of myosins, is expressed in the retina. Its deletion was previously shown to reduce amplitudes of the a- and b-waves of the electroretinogram. Analyzing wild-type and myosin VI-deficient Snell's Waltzer mice in more detail, the expression pattern of myosin VI in retinal pigment epithelium, outer limiting membrane, and outer plexiform layer could be linked with differential progressing ocular deficits. These encompassed reduced a-waves and b-waves and disturbed oscillatory potentials in the electroretinogram, photoreceptor cell death, retinal microglia infiltration, and formation of basal laminar deposits. A phenotype comprising features of glaucoma (neurodegeneration) and age-related macular degeneration could thus be uncovered that suggests dysfunction of myosin VI and its variable cargo adaptor proteins for membrane sorting and autophagy, as possible candidate mediators for both disease forms.Cellular and Molecular Life Sciences CMLS 05/2015; DOI:10.1007/s00018-015-1913-3 · 5.86 Impact Factor