Glaucoma: Neurodegenerative Disease of the Retina and Beyond Part A pdf free Glaucoma is a neurodegenerative disease of the visual system characterized by the progressive death of retinal ganglion cells (RGCs) and the loss of their axons that form the optic nerve. Increased intraocular pressure (IOP) has been demonstrated to be the main risk factor associated with the onset and progression of the disease. Despite medical and surgical approaches to reducing IOP is available, actually, this disease is one of the major causes of blindness in the world.
Over the last decade, dissection under normal and pathological conditions of molecular mechanisms implicated in the control of cell survival and demise and interplay among retinal cells of diverse embryologic origin have widened the perspective for developing neuroprotective therapeutic approaches other than IOP control in glaucoma. Accordingly, considerable interest has been recently directed toward the identification of novel therapeutic strategies based upon neuroprotection. In this issue of Progress in Brain Research dedicated to glaucoma, leaders in this scientific field have discussed their original and innovative data as well as data originated from the clinic. In view of the large collection yielded, this latter effort has been reported in two separate volumes. The first volume (256) is dedicated to the wealth of mechanisms underlying the neuronal damage in glaucoma. In particular, the reader is introduced to the potential contribution of altered fundamental cellular mechanisms (see autophagy) as well as microbial dysbiosis through the modulation of adaptive immunity. The more extensively dissected role of innate immunity via microglia activation and soluble neuroinflammatory mediators release in retinal ganglion cells as well as the contribution of oxidative stress are deeply explored. This latter may contribute to the observed alterations of the cerebrospinal fluid dynamic and/or composition that may play a role in the pathogenesis of glaucoma. Glaucoma: Neurodegenerative Disease of the Retina and Beyond part A pdf free volume 256 you can download it in this post later.
|Book Name||Neurodegenerative Disease of the Retina and Beyond|
|Author of Book||Giacinto Bagetta (Editor)|
What is Neurodegenerative
Before moving ahead we need to understand basically what is Neurodegenerative.
Neurodegenerative diseases are incurable and debilitating conditions that cause progressive degeneration and / or death of nerve cells. This causes problems with movement (called ataxias) or mental functioning (called dementias).
More than 60 million people worldwide are diagnosed with glaucomatous optic neuropathy, which is estimated to be responsible for 8.4 million cases of irreversible blindness worldwide. Glaucoma is associated with characteristic optic nerve damage and visual field loss patterns that primarily involve the loss of retinal ganglion cells (RGC). At present, intraocular pressure (IOP) presents the only modifiable risk factor for glaucoma, although WCR and vision loss may continue in patients despite well-controlled IOP. This, together with the current inability to diagnose glaucoma until a relatively advanced stage of the disease process, has led to intensive research towards the development of novel techniques for the early diagnosis of the disease.
This review describes our current understanding of the possible mechanisms underlying RGC and axonal loss in glaucoma. The similarities between glaucoma and other neurodegenerative diseases of the central nervous system are established before providing an overview of recent developments in RGC health monitoring techniques, including recent progress towards the development of RGC-specific contrast agents. The review concludes by discussing techniques to assess glaucomatous changes in the brain using MRI and the clinical relevance of glaucoma-associated changes in the visual centers of the brain.
Here is the preface of Glaucoma: Neurodegenerative Disease of the Retina and Beyond part A pdf free volume 256. Particularly interesting are the data reported in the second volume starting with a chapter devoted to the use of artificial intelligence in the diagnosis and therapy of glaucoma. There are many variables that affect the early diagnosis of the disease and the monitoring of its progression; the introduction of artificial intelligence in clinical practice could greatly support the work of ophthalmologists. Data supporting the hypothesis that glaucoma may be influenced by or may share common pathogenic mechanisms with diseases of the central nervous system (CNS) have been accumulated.
In agreement with the latter, evidence exists suggesting that the central nervous pathways damaged in glaucoma may play a role in sustaining functional and daily living disability caused by the disease. This second volume incorporates a meta-analysis on the clinical evidence of the neuroprotective properties of brimonidine and current scrutiny of naturally occurring potential neuroprotectants. An outlook to future strategies for glaucoma neuroprotection is also proposed. In fact, a chapter overviews the current progress on the regeneration of pluripotent stem cell-derived RGCs and outlooks the perspective in this field.
We would like to acknowledge the outstanding contribution of all the authors to the success of these volumes of Progress in Brain Research dedicated to glaucoma and the excellent collaboration of the highly professional staff of Elsevier. In particular, we would like to acknowledge the constant and skillful support of Mr. Hilal Johnson throughout the whole editorial process. Finally, we would also thank the Referees who have contributed a great deal to improve our editorial work.
To study short and long-term effects of acute ocular hypertension (AOHT) on inner and outer retinal layers, in adult Sprague-Dawley rats AOHT (87mmHg) was induced for 90min and the retinas were examined longitudinally in vivo with electroretinogram (ERG) recordings and optical coherent tomography (OCT) from 1 to 90 days (d). Ex vivo, the retinas were analyzed for rod (RBC) and cone (CBC) bipolar cells, with antibodies against protein kinase Cα and recoverin, respectively in cross-sections, and for cones, horizontal (HZ) and ganglion (RGC) cells with antibodies against arrestin, calbindin and Brn3a, respectively in whole mounts. The inner retina thinned progressively up to 7 d with no further changes, while the external retina had a normal thickness until 30 d, with a 20% thinning between 30 and 90 d.
Functionally, the a-wave showed an initial reduction by 24 h and a further reduction from 30 to 90 d. All other main ERG waves were significantly reduced by 1 d without significant recovery by 90 d. Radial sections showed a normal population of RBCs but their terminals were reduced. The CBCs showed a progressive decrease with a loss of 56% by 30 d. In wholemount retinas, RGCs diminished to 40% by 3 d and to 16% by 30 d without further loss. Cones diminished to 58% and 35% by 3 and 7 d, respectively and further decreased between 30 and 90 d. HZs showed normal values throughout the study. In conclusion, AOHT affects both the inner and outer retina, with a more pronounced degeneration of the cone than the rod pathway.
Acute ocular hypertension, Glaucoma, Rat retina, Bipolar cells, Horizontal cells, Cones,
Retinal ganglion cells, Transient retinal ischemia
What is Glaucoma
Glaucoma is an optic neuropathy characterized by the progressive loss of retinal ganglion cells (RGC) with concomitant visual field deficits that can progress silently to advanced stages of the disease (Leite et al., 2011) and is the main cause of irreversible blindness (Quigley, 2006). ). Additional hallmarks of glaucoma include structural abnormalities of the nerve fiber layer and the optic disc (Chauhan et al., 2014; Weinreb et al., 2014).
Independent research from various laboratories has shown that glaucoma is not only a disease of the inner retina, but also of the main retinofugal pathway. It has become clear in studies of human glaucoma and experimental models of ocular hypertension that this disease also affects the main relay nuclei of the thalamic and midbrain (Dekeyster et al., 2015; ValienteSoriano et al., 2015a; Y € ucel, 2003 ; Y € ucel. And Gupta, 2008), as well as the primary (Nucci et al., 2013) and associated (Frezzotti et al., 2014) areas of the visual cortex. Furthermore, growing evidence indicates that the pre-ganglion cell circuit of the visual pathway is also affected both functionally and structurally (Mittag et al., 2000; Nork et al., 2000; Ortı´n-Martı´nez et al. ., 2015).
Thus, glaucoma can be considered today a disease of the entire primary visual pathway that begins somewhere near the head of the optic nerve, from where it progresses towards the cortical areas and backwards in a more prolonged way towards the photoreceptors (VidalSanz et al., 2012, 2015a, 2017). Although the pathology of glaucoma is not fully understood, it is generally accepted that it is a multifactorial neurodegenerative disease in which axonal compression, vascular dysfunction, oxidative stress, immune neuroinflammation, and ischemia (Burgoyne, 2015; Flammer et al., 2002; Tezel et al., 2002; Tezel et al., 2002). al., 2010) may play a role. Consequently, several studies have investigated the effects of axotomy, excitotoxicity, oxidative stress, inflammation, and immune-related ischemia in an effort to understand the pathophysiology of glaucoma.
Intraorbital optic nerve injury is a classic model that allows studying plasticity, that is, axonal regeneration (Aguayo et al., 1987; Bray et al., 1987), target reinnervation (Avil es-Trigueros et al., 2000; Vidal-Sanz et al., 1987, 2002) synapse formation (Keirstead et al., 1989; Vidal-Sanz et al., 1987, 1991; Whiteley et al., 1998) as well as neuroprotection (Lindqvist et al. , 2004; L € onngren et al., 2006; Vidal-Sanz et al., 2007) of the visual system of adult mammals. In addition, optic nerve injury (ON) has allowed a detailed characterization of the effects of axotomy in adult rats and mice after crushing or complete transection (Nadal-Nicola et al., 2015, 2017; Sa´nchezMigallo´n et al., 2018; Villegas-Pérez et al., 1993) of intraorbital ON. These studies have shown that after axotomy there is a rapid loss of RGC followed by a more protracted RGC death that occurs over the following months with a very small proportion of RGC surviving long after injury.
You can also read this Neurodegenerative Disease book here online free
Here you can download the 256 volume of Glaucoma: Neurodegenerative Disease of the Retina and Beyond Part A in pdf format with a direct download link of google drive. I always try to post easy and free downloadable content. Don’t forget to share with others.