Bilateral Basal Nuclei Vacuolar Lesions: A Novel and Emerging Potential Background Finding in Beagle Dogs.

In this case presentation, the speaker and co-authors represented a group of scientists engaged in a cross-institutional precompetitive working group focused on elucidating a novel background change in the basal nuclei of Beagle dogs. The group's ongoing efforts since first publication of the lesion in 2024 enabled further characterization of the lesion and revealed additional incidences in control animals. The characterization, including newly discovered lesion features, and terminology of the condition were outlined and suggestions for interpretation in nonclinical toxicity studies were given.

A method to identify, dissect and stain equine neuromuscular junctions for morphological analysis.

Morphological study of the neuromuscular junction (NMJ), a specialised peripheral synapse formed between a lower motor neuron and skeletal muscle fibre, has significantly contributed to the understanding of synaptic biology and neuromuscular disease pathogenesis. Rodent NMJs are readily accessible, and research into conditions such as amyotrophic lateral sclerosis (ALS), Charcot-Marie-Tooth disease (CMT), and spinal muscular atrophy (SMA) has relied heavily on experimental work in these small mammals. However, given that nerve length dependency is an important feature of many peripheral neuropathies, these rodent models have clear shortcomings; large animal models might be preferable, but their size presents novel anatomical challenges.

Recognising the potential of large animals for modelling neuromuscular junction physiology and disease.

The aetiology and pathophysiology of many diseases of the motor unit remain poorly understood and the role of the neuromuscular junction (NMJ) in this group of disorders is particularly overlooked, especially in humans, when these diseases are comparatively rare. However, elucidating the development, function and degeneration of the NMJ is essential to uncover its contribution to neuromuscular disorders, and to explore potential therapeutic avenues to treat these devastating diseases. Until now, an understanding of the role of the NMJ in disease pathogenesis has been hindered by inherent differences between rodent and human NMJs: stark contrasts in body size and corresponding differences in associated axon length underpin some of the translational issues in animal models of neuromuscular disease.

BDNF-dependent modulation of axonal transport is selectively impaired in ALS.

Axonal transport ensures long-range delivery of essential cargoes between proximal and distal compartments, and is needed for neuronal development, function, and survival. Deficits in axonal transport have been detected at pre-symptomatic stages in the SOD1 and TDP-43 mouse models of amyotrophic lateral sclerosis (ALS), suggesting that impairments in this critical process are fundamental for disease pathogenesis. Strikingly, in ALS, fast motor neurons (FMNs) degenerate first whereas slow motor neurons (SMNs) are more resistant, and this is a currently unexplained phenomenon.

Sinonasal mycosis following transfrontal craniotomy in three dogs.

Case Description: Three dogs were presented for investigation of chronic nasal discharge and epistaxis 141, 250, and 357 days after undergoing transfrontal craniotomy to treat an intracranial meningioma (2 dogs) or a meningoencephalocele (1 dog).

Clinical Findings: CT findings were consistent with destructive rhinitis and frontal sinusitis in all 3 dogs, with results of histologic examination and fungal culture of samples obtained during frontal sinusotomy confirming mycotic infection. Frontal sinusotomy revealed fungal plaques covering a combination of bone and residual surgical tissue adhesive at the site of the previous craniotomy in all 3 dogs.

Optimisation and validation of immunohistochemical axonal markers for morphological and functional characterisation of equine peripheral nerves.

Background: Horses are affected by various peripheral nerve disorders but defining their aetiology and pathophysiology is hampered by limited understanding of associated morphological and pathological changes and involvement of specific axonal types.

Objectives: To investigate the hypothesis that selected antibody markers, used in conjunction with various tissue processing methods, would enable identification of axons with different functional modalities within a range of equine peripheral nerves.

Study Design: Optimisation and validation study.

Assessing pathological changes within the nucleus ambiguus of horses with recurrent laryngeal neuropathy: An extreme, length-dependent axonopathy.

Introduction: Equine recurrent laryngeal neuropathy (RLN) is a naturally occurring model of length-dependent axonopathy characterized by asymmetrical degeneration of recurrent laryngeal nerve axons (RLn). Distal RLn degeneration is marked, but it is unclear whether degeneration extends to include cell bodies (consistent with a neuronopathy).

Methods: With examiners blinded to RLN severity, brainstem location, and side, we examined correlations between RLN severity (assessed using left distal RLn myelinated axon count) and histopathological features (including chromatolysis and glial responses) in the nucleus ambiguus cell bodies, and myelinated axon count of the right distal RLn of 16 horses.

Oesophageal angioleiomyosarcoma in a cat.

A female spayed domestic longhair cat aged 3 years and 9 months was referred for investigation of regurgitation and weight loss of 2 months' duration. Thoracic radiographs revealed a soft tissue mass within the cranial mediastinum causing focal oesophageal dilation. Computed tomography confirmed a contrast-enhancing mass located cranial to the heart base, possibly originating from the oesophagus.

Malignant melanoma in a grey horse: case presentation and review of equine melanoma treatment options.

A 15 year-old grey Thoroughbred gelding presented for investigation of chronic weight loss and recent onset of respiratory difficulty. Clinical examination confirmed tachypnoea with increased respiratory effort. Thoracic ultrasound examination detected pleural effusion.

Targeted suppression of claudin-5 decreases cerebral oedema and improves cognitive outcome following traumatic brain injury.

Traumatic brain injury is the leading cause of death in children and young adults globally. Malignant cerebral oedema has a major role in the pathophysiology that evolves after severe traumatic brain injury. Added to this is the significant morbidity and mortality from cerebral oedema associated with acute stroke, hypoxic ischemic coma, neurological cancers and brain infection.