Glial Response and Neuroinflammation in Cerebrocortical Atrophy in a Young Irish Wolfhound Dog

Fabiano José Ferreira De Sant’ana ,Ester Blasco,Miguel Omaña,M Pumarola

doi:10.3390/ani11010143

Abstract

Simple SummaryNeuroinflammation is considered a reaction of the nervous system itself to protect and repair structural changes developed in it. Despite its initial positive purpose, sometimes it can produce worse consequences for the tissue. In this article, we present a case of an Irish Wolfhound dog suffering a rare idiopathic neurodegenerative disease producing wide cerebral cortical damage with loss of neuronal bodies in a bilateral and symmetrical pattern. We have studied the glial components of the neuroinflammation developed describing how they have exacerbated the nervous tissue damage.A two-year-old, Irish Wolfhound dog presented with a history of progressive neurological signs. Neurological exam revealed disorientation, absence of menace response, reduction of right nasal sensation, hypermetria and ataxia with reduction of proprioception in all four limbs. MRI findings were compatible with laminar neuronal necrosis and possible bilateral cortical cerebral atrophy. Grossly, a severe bilateral reduction of the gray matter with flattening of gyri, mainly in frontal and parietal cerebral areas, was observed. Histologically, multiple, segmental, bilateral, and symmetric areas of neuronal loss, necrosis and degeneration, in a laminar pattern, associated with a reactive gliosis were observed. Immunohistochemical studies showed severe reduction of neuronal bodies, proliferation and hypertrophy of astrocytes and microglia. Few perivascular B and T cells were demonstrated. Based on these data, we show some of the neuroinflammatory events that occur during CNS repair in a chronic phase of this condition.

Highlights

Degenerative neurological diseases in domestic animals include a broad group of disorders that are characterized by progressive, bilateral and symmetrical degeneration and loss of cells, mainly neurons
The positive controls for IHC consisted of brain (NeuN, Glial Fibrillary Acidic Protein (GFAP), and Iba-1) and lymph node (CD3 and CD20) of a dog without morphologic
Tbsheerpveodsi.tive controls for IHC consisted of brain (NeuN, GFAP, and Iba-1) and lymph node (CD3 and CD20) of a dog without morphologic changes

Summary

Introduction

Degenerative neurological diseases in domestic animals include a broad group of disorders that are characterized by progressive, bilateral and symmetrical degeneration and loss of cells, mainly neurons Most of these diseases are of a genetic basis, but the precise pathogenic mechanisms are still poorly known or understood. Neuroinflammation, the activation of the neuroimmune cells (microglia and astrocytes) into proinflammatory states, with no known causative insult and little change in blood-brain barrier biology, has been suggested as a pathological contributor in several neurodevelopmental, psychiatric, and neurodegenerative disorders [3] This sustained inflammatory response suggests an important role of effectors of neuroinflammation in neuronal dysfunction and death [4]. We describe the pathological and immunohistochemical findings in one case of cerebrocortical atrophy in a young Irish Wolfhound dog, with emphasis on the glial reaction (neuroinflammation) and on the poor lymphocytic response to neuronal injury, which has not been previously investigated

Description of the Case

DDiissccuussssiioonn

Conclusions