The existence of neuroinflammation and oxidative stress surrounding amyloid beta (Aβ) plaques, a hallmark of Alzheimer’s disease (AD), has been demonstrated and may result in the activation of neuronal death and inhibition of neurogenesis. Therefore, dysregulation of neuroinflammation and oxidative stress is one possible therapeutic target for AD. Kaempferia parviflora Wall. ex Baker (KP), a member of the Zingiberaceae family, possesses health-promoting benefits including anti-oxidative stress and anti-inflammation in vitro and in vivo with a high level of safety; however, the role of KP in suppressing Aβ-mediated neuroinflammation and neuronal differentiation has not yet been investigated. The neuroprotective effects of KP extract against Aβ₄₂ have been examined in both monoculture and co-culture systems of mouse neuroectodermal (NE-4C) stem cells and BV-2 microglia cells. Our results showed that fractions of KP extract containing 5,7-dimethoxyflavone, 5,7,4′-trimethoxyflavone, and 3,5,7,3′,4′-pentamethoxyflavone protected neural stem cells (both undifferentiated and differentiated) and microglia activation from Aβ₄₂-induced neuroinflammation and oxidative stress in both monoculture and co-culture system of microglia and neuronal stem cells. Interestingly, KP extracts also prevented Aβ₄₂-suppressed neurogenesis, possibly due to the contained methoxyflavone derivatives. Our data indicated the promising role of KP in treating AD through the suppression of neuroinflammation and oxidative stress induced by Aβ peptides.

Background: Canine cognitive dysfunction syndrome (CCDS) is a progressive neurodegenerative disorder found in senior dogs. Due to the lack of biological markers, CCDS is commonly underdiagnosed. The aim of this study was to identify potential plasma biomarkers using proteomics techniques and to increase our understanding of the pathogenic mechanism of the disease. Plasma amyloid beta 42 (Aβ₄₂) has been seen to be a controversial biomarker for CCDS. Proteomics analysis was performed for protein identification and quantification. Results: Within CCDS, ageing, and adult dogs, 87 proteins were identified specific to Canis spp. in the plasma samples. Of 87 proteins, 48 and 41 proteins were changed in the ageing and adult groups, respectively. Several distinctly expressed plasma proteins identified in CCDS were involved in complement and coagulation cascades and the apolipoprotein metabolism pathway. Plasma Aβ₄₂ levels considerably overlapped within the CCDS and ageing groups. In the adult group, the Aβ₄₂ level was low compared with that in the other groups. Nevertheless, plasma Aβ₄₂ did not show a correlation with the Canine Cognitive Dysfunction Rating scale (CCDR) score in the CCDS group (p = 0.131, R² = 0.261). Conclusions: Our present findings suggest that plasma Aβ₄₂ does not show potential for use as a diagnostic biomarker in CCDS. The nano-LC-MS/MS data revealed that the predictive underlying mechanism of CCDS was the co-occurrence of inflammation-mediated acute phase response proteins and complement and coagulation cascades that partly functioned by apolipoproteins and lipid metabolism. Some of the differentially expressed proteins may serve as potential predictor biomarkers along with Aβ₄₂ in plasma for improved CCDS diagnosis. Further study in larger population-based cohort study is required in validation to define the correlation between protein expression and the pathogenesis of CCDS.

Acute pancreatitis is a common condition in dogs associated with significant diagnostic and management challenges. Although current treatments largely provide supportive and symptomatic care, a more profound understanding of the metabolic response of canine acute pancreatitis might facilitate the development of more targeted interventions. This study characterized the plasma metabolomic profile of dogs with acute pancreatitis. Twelve dogs, including six clinically diagnosed with acute pancreatitis and six healthy controls, were investigated. Plasma samples were analyzed using liquid chromatography-tandem mass spectrometry, and the resulting metabolomic data were assessed using partial least squares discriminant analysis, revealing clear separation between the groups. Pathway analysis identified significant alterations in glycine, serine, and threonine metabolism; histidine metabolism; and arginine biosynthesis, with additional trends observed in nitrogen metabolism. Five metabolites displayed diagnostic relevance, with γ-glutamylmethionine, 4-hydroxynonenal-glutathione, γ-glutamylalanine, and pyrocatechol levels being significantly reduced in dogs with acute pancreatitis (all p < 0.001) and N-acetyl-Leu levels being significantly elevated (p < 0.001). These metabolites demonstrated strong discriminatory power, and they represent potential biomarkers for canine acute pancreatitis, particularly reflecting oxidative stress, inflammation, and altered amino acid metabolism. Further research is warranted to validate their clinical utility and explore their mechanistic roles in the pathophysiology of acute pancreatitis, potentially guiding future diagnostic and therapeutic innovations in veterinary medicine.

The prevalence of neurological disorders (NDs) such as Alzheimer's disease (AD) is increasing globally, and the lack of effective pharmacological interventions presents a significant health risk. Multiple mechanisms including the activation of oxidative stress, amyloid pathway, ER stress, and neuroinflammation have been implicated in AD; therefore, multi-targeted agents against these mechanisms may be preferable to single-target agents. Phikud Navakot (PN), a Thai traditional medicine combining nine herbs, has been shown to reduce oxidative stress and neuroinflammation of neuronal and microglia cells and the coculture between them, indicating the promising role of PN extract as anti-AD. This study evaluated the neuroprotective effects of PN extract against oxidative stress, amyloid pathway, endoplasmic reticulum stress (ER stress), and neuroinflammation using neuronal and microglia cells, as well as in a Drosophila model of AD. Results showed that PN extract reduced oxidative stress, lipid peroxidation, pro-inflammatory cytokines, amyloid pathway, and ER stress induced by aluminum chloride (AlCl₃, AD-induced agent) or thapsigargin (TG, an ER stress activator) in both neurons and microglia cells. PN extract also reduced oxidative stress, ER-stress-related genes, and neurotoxic peptides (amyloid beta) in a Drosophila model of AD. Data indicated that PN extract may function as an anti-AD agent by targeting multiple mechanisms as described. This research also revealed for the first time that PN extract acted as an ER stress inhibitor.