Publications by authors named "Davor Virag"

Article Synopsis
  • Parkinson's disease (PD) exhibits a wide range of symptoms, complicating the translation of treatment efficacy from animal models to humans, suggesting that current models may not fully capture all PD characteristics.
  • This project investigates whether metabolic dysfunction, induced by administering streptozotocin directly into the striatum of rats, can mimic the symptoms of PD typically seen in patients, focusing on cognitive and motor functions.
  • Results showed that rats given streptozotocin bilaterally experienced significant motor and cognitive impairments alongside disrupted brain metabolism, indicating that this method could provide a better animal model for studying PD and testing new therapies.
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Recent evidence suggests that the gut plays a vital role in the development and progression of Alzheimer's disease (AD) by triggering systemic inflammation and oxidative stress. The well-established rat model of AD, induced by intracerebroventricular administration of streptozotocin (STZ-icv), provides valuable insights into the GI implications of neurodegeneration. Notably, this model leads to pathophysiological changes in the gut, including redox dyshomeostasis, resulting from central neuropathology.

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The gut-brain axis plays an important role in Parkinson's disease (PD) by acting as a route for vagal propagation of aggregated α-synuclein in the gut-first endophenotype and as a mediator of gastrointestinal dyshomeostasis via the nigro-vagal pathway in the brain-first endophenotype of the disease. One important mechanism by which the gut-brain axis may promote PD is by regulating gastrointestinal redox homeostasis as overwhelming evidence suggests that oxidative stress plays a key role in the etiopathogenesis and progression of PD and the gastrointestinal tract maintains redox homeostasis of the organism by acting as a critical barrier to environmental and microbiological electrophilic challenges. The present aim was to utilize the bilateral intrastriatal 6-hydroxydopamine (6-OHDA) brain-first PD model to study the effects of isolated central pathology on redox homeostasis of the gastrointestinal tract.

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Sarcopenia is a process of progressive aging-associated loss of skeletal muscle mass (SMM) recognized as a serious global health issue contributing to frailty and increased all-cause mortality. Exercise and nutritional interventions (particularly intake of dairy products and milk) demonstrate good efficacy, safety, and broad applicability. Here, we propose that at least some of the well-documented favorable effects of milk and milk-derived protein supplements on SMM might be mediated by D-galactose, a monosaccharide present in large quantities in milk in the form of disaccharide lactose (milk sugar).

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The gut might play an important role in the etiopathogenesis of Alzheimer's disease (AD) as gastrointestinal alterations often precede the development of neuropathological changes in the brain and correlate with disease progression in animal models. The gut has an immense capacity to generate free radicals whose role in the etiopathogenesis of AD is well-known; however, it remains to be clarified whether gastrointestinal redox homeostasis is associated with the development of AD. The aim was to (i) examine gastrointestinal redox homeostasis in the presymptomatic and symptomatic Tg2576 mouse model of AD; (ii) investigate the effects of oral d-galactose previously shown to alleviate cognitive deficits and metabolic changes in animal models of AD and reduce gastrointestinal oxidative stress; and (iii) investigate the association between gastrointestinal redox biomarkers and behavioral alterations in Tg2576 mice.

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The gastrointestinal (GI) system is affected in Alzheimer's disease (AD); however, it is currently unknown whether GI alterations arise as a consequence of central nervous system (CNS) pathology or play a causal role in the pathogenesis. GI mucus is a possible mediator of GI dyshomeostasis in neurological disorders as the CNS controls mucus production and secretion via the efferent arm of the brain-gut axis. The aim was to use a brain-first model of sporadic AD induced by intracerebroventricular streptozotocin (STZ-icv; 3 mg/kg) to dissect the efferent (i.

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Type 2 diabetes mellitus increases the risk of sporadic Alzheimer's disease (sAD), and antidiabetic drugs, including the sodium-glucose cotransporter inhibitors (SGLTI), are being studied as possible sAD therapy. We have explored whether the SGLTI phloridzin may influence metabolic and cognitive parameters in a rat model of sAD. Adult male Wistar rats were randomized to a control (CTR), an sAD-model group induced by intracerebroventricular streptozotocin (STZ-icv; 3 mg/kg), a CTR+SGLTI, or an STZ-icv+SGLTI group.

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Cognitive deficit is a frequent non-motor symptom in Parkinson's disease (PD) with an unclear pathogenesis. Recent research indicates possible involvement of insulin resistance and glutamate excitotoxicity in PD development. We investigated cognitive performance and the brain glutamate and insulin signaling in a rat model of PD induced by bilateral intrastriatal injection of 6-hydroxydopamine (6-OHDA).

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Article Synopsis
  • Alzheimer's disease (AD) is primarily a sporadic condition largely linked to the APOE ε4 gene, with limited disease-modifying treatments available, mainly aducanumab and lecanemab.
  • Attention-deficit hyperactivity disorder (ADHD) is common in children and persists into adulthood for many, with its treatment relying on first-line stimulants like methylphenidate (MPH) but lacking definitive disease-modifying therapies.
  • Research suggests potential links between ADHD and AD, including shared cognitive deficits and biological pathways, indicating that ADHD might increase the risk for developing AD and that treatments for ADHD might benefit cognitive function in early stages of dementia.
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Background: Assessment of neuromuscular function is critical for understanding pathophysiological changes related to motor system dysfunction in many rodent disease models. Among methods used for quantification of grip performance in rodents, gauge-based grip strength meters provide the most reliable results, however, such instruments are unaffordable by many laboratories. The present aim was to demonstrate how to build a rodent grip strength apparatus from scratch using a digital kitchen scale, an empty cage, and a microcontroller, with both hardware and software being completely open-source to enable maximal modularity and flexibility of the instrument in concordance with the principles of open-source bioinstrumentation.

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Unlabelled: COVID-19-related (vs. non-related) articles appear to be more expeditiously processed and published in peer-reviewed journals. We aimed to evaluate: (i) whether COVID-19-related preprints were favored for publication, (ii) preprinting trends and public discussion of the preprints, and (iii) the relationship between the publication topic (COVID-19-related or not) and quality issues.

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Galactose is a ubiquitous monosaccharide with important yet incompletely understood nutritive and physiological roles. Chronic parenteral d-galactose administration is used for modeling aging-related pathophysiological processes in rodents due to its ability to induce oxidative stress (OS). Conversely, chronic oral d-galactose administration prevents and alleviates cognitive decline in a rat model of sporadic Alzheimer's disease, indicating that galactose may exert beneficial health effects by acting in the gut.

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Article Synopsis
  • The proposed method measures the reductive capacity of biological samples using potassium permanganate reduction and trapping manganese dioxide on a nitrocellulose membrane.* -
  • Nitrocellulose redox permanganometry (NRP) is a quick and cost-effective technique that allows for the high-throughput analysis of both liquid and solid biological samples.* -
  • HistoNRP, a modified version of NRP, enables detailed spatial analysis of reductive capacity in tissue samples while preserving their anatomical structure.*
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Article Synopsis
  • Galactose, a common sugar, might help with aging and cognitive problems in rats, as recent studies show it maintains cell function during starvation and could be beneficial in Alzheimer's disease models.
  • Researchers tested the effects of galactose on rat brain chemistry, finding no major systemic imbalance but a slight increase in oxidative stress and an unexpected rise in the brain’s ability to counteract this stress.
  • The study suggests that galactose may have protective, yet paradoxically pro-oxidative, effects at a biochemical level, leading to a new hypothesis that it could be both beneficial and slightly harmful.
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