Experimental colitis in young Tg2576 mice accelerates the onset of an Alzheimer’s-like clinical phenotype DOI Creative Commons
Luca Lorenzini,

Lorenzo Zanella,

Michele Sannia

et al.

Alzheimer s Research & Therapy, Journal Year: 2024, Volume and Issue: 16(1)

Published: May 21, 2024

Abstract Systemic inflammation and neuroinflammation affect the natural course of sporadic form Alzheimer’s disease (AD), as supported by epidemiological preclinical data, several studies indicate a higher prevalence AD in patients with inflammatory bowel disease. In this study, we explored whether colitis induced dextran sulfate sodium (DSS) young, presymptomatic/preplaque mice worsens and/or anticipates age-dependent cognitive impairment Tg2576, widely used mouse model AD. We demonstrated that DSS young Tg2576 onset age learning memory deficit Morris water maze test. To explore potential mechanisms behind acceleration decline colitis, focused on gut microbiota, systemic markers. observed Firmicutes/Bacteroidetes ratio change animals comparable to elderly mice, suggesting accelerated microbiota aging not C57BL6 mice. also substantial differences between WT neuroinflammation-related parameters early 3 months age, well before plaque deposition, picture which evolved rapidly (between 5.5 age) contrast littermates treated DSS. detail, following induction exhibited contrasting features expression level inflammation-evoked astrocyte-associated genes hippocampus. No changes microglial occurred hippocampus experimental groups, whereas reduced glial fibrillary acidic protein immunoreactivity was vs. This finding may reflect an atrophic, “loss-of-function” profile, further exacerbated where decreased GFAP mRNA detected. conclusion, suggest as-yet unidentified peripheral mediators evoked involving gut-brain axis emphasize astrocyte profile present leading impaired synaptic morphological functional integrity very sign

Language: Английский

Nootropic foods in neurodegenerative diseases: mechanisms, challenges, and future DOI Creative Commons
Le Anh Minh Nguyen, Courtney Wayne Simons, Raymond Thomas

et al.

Translational Neurodegeneration, Journal Year: 2025, Volume and Issue: 14(1)

Published: April 3, 2025

Neurodegenerative diseases (NDDs) such as Alzheimer's and Parkinson's disease are increasing globally represent a significant cause of age-related death in the population. Recent studies emphasize strong association between environmental stressors, particularly dietary factors, brain health neurodegeneration unsatisfactory outcomes. Despite ongoing efforts, efficiency current treatments for NDDs remains wanting. Considering this, nootropic foods with neuroprotective effects high interest part possible long-term therapeutic strategy to improve alleviate NDDs. However, since it is new emerging area food neuroscience, there limited information on mechanisms challenges consider this be successful intervention. Here, we seek address these gaps by presenting comprehensive review pathways or including mutual interactions governing metabolism, linkages NDDs, intake, properties foods. We also discuss in-depth intervention compounds patterns providing detailed exploration their action. Additionally, analyze demand, challenges, future directions development targeting

Language: Английский

Citations

0

Investigating interleukin-8 in Alzheimer's disease: A comprehensive review DOI
Delia Righi, Carlo Manco, Matteo Pardini

et al.

Journal of Alzheimer s Disease, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 18, 2024

Several studies indicate that the development of Alzheimer's disease (AD) has strong interactions with immune mechanisms within brain, indicating a close association between inflammation in central nervous system and progression neurodegeneration. Despite considerable progress understanding inflammatory aspects AD, several them remain unresolved. Pro-inflammatory cytokines microglia are pivotal components cascade. Among these, role interleukin-8 (IL-8) neurodegeneration seems complex multifaceted, involving inflammation, neurotoxicity, blood-brain barrier disruption, oxidative stress, is still poorly characterized. We conducted review to describe evidence IL-8 involvement AD. cytokine known for its proinflammatory properties typically produced by macrophages, predominantly functions as chemotactic signal attracting neutrophils inflamed sites bloodstream. Interestingly, also present where it primarily released response signals. This aims provide comprehensive overview structure, function, regulatory relevant AD pathology.

Language: Английский

Citations

3

Anesthesia‐induced hippocampal‐cortical hyperactivity and tau hyperphosphorylation impair remote memory retrieval in Alzheimer's disease DOI Creative Commons
Kai Chen, Riya Gupta, Alejandro Martín‐Ávila

et al.

Alzheimer s & Dementia, Journal Year: 2023, Volume and Issue: 20(1), P. 494 - 510

Published: Sept. 11, 2023

Abstract INTRODUCTION Anesthesia often exacerbates memory recall difficulties in individuals with Alzheimer's disease (AD), but the underlying mechanisms remain unclear. METHODS We used vivo Ca 2+ imaging, viral‐based circuit tracing, and chemogenetic approaches to investigate anesthesia‐induced remote impairment mouse models of presymptomatic AD. RESULTS Our study identified pyramidal neuron hyperactivity anterior cingulate cortex (ACC) as a significant contributor impairment. This ACC hyperactivation arises from disinhibition local inhibitory circuits increased excitatory inputs hippocampal CA1 region. Inhibiting CA1‐ACC improved after anesthesia. Moreover, anesthesia led tau phosphorylation hippocampus, inhibiting this hyperphosphorylation prevented subsequent DISCUSSION Hippocampal‐cortical plays role Targeting shows promise therapeutic strategy mitigate neural network dysfunction retrograde amnesia

Language: Английский

Citations

7

Early postoperative cognitive decline—are there any preventive strategies for surgical patients in the emergency setting? DOI Open Access

Ana-Maria Cotae,

Liliana Mirea, Cristian Cobilinschi

et al.

Signa Vitae, Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 1, 2024

Postoperative neurocognitive impairments following surgery are a growing concern, especially in the elderly population, since it is associated with significantly increased risk of morbi-mortality postoperative period. Among them, delirium or early cognitive decline further prolonged dysfunction and may quicken long-term impairment (POCD). The current knowledge regarding preventive strategies for not focused anymore only on pharmacological behavioral management period, but also supports preoperative training programs. Since evaluation proactive interventions to optimize surgical patient outcomes rather impossible emergency setting, what appropriate that can be implemented day-to-day practice? In this review, we try highlight most recent experimental clinical strategies, outline relevant recommendations clinicial practicioners based available data.

Language: Английский

Citations

2

Experimental colitis in young Tg2576 mice accelerates the onset of an Alzheimer’s-like clinical phenotype DOI Creative Commons
Luca Lorenzini,

Lorenzo Zanella,

Michele Sannia

et al.

Alzheimer s Research & Therapy, Journal Year: 2024, Volume and Issue: 16(1)

Published: May 21, 2024

Abstract Systemic inflammation and neuroinflammation affect the natural course of sporadic form Alzheimer’s disease (AD), as supported by epidemiological preclinical data, several studies indicate a higher prevalence AD in patients with inflammatory bowel disease. In this study, we explored whether colitis induced dextran sulfate sodium (DSS) young, presymptomatic/preplaque mice worsens and/or anticipates age-dependent cognitive impairment Tg2576, widely used mouse model AD. We demonstrated that DSS young Tg2576 onset age learning memory deficit Morris water maze test. To explore potential mechanisms behind acceleration decline colitis, focused on gut microbiota, systemic markers. observed Firmicutes/Bacteroidetes ratio change animals comparable to elderly mice, suggesting accelerated microbiota aging not C57BL6 mice. also substantial differences between WT neuroinflammation-related parameters early 3 months age, well before plaque deposition, picture which evolved rapidly (between 5.5 age) contrast littermates treated DSS. detail, following induction exhibited contrasting features expression level inflammation-evoked astrocyte-associated genes hippocampus. No changes microglial occurred hippocampus experimental groups, whereas reduced glial fibrillary acidic protein immunoreactivity was vs. This finding may reflect an atrophic, “loss-of-function” profile, further exacerbated where decreased GFAP mRNA detected. conclusion, suggest as-yet unidentified peripheral mediators evoked involving gut-brain axis emphasize astrocyte profile present leading impaired synaptic morphological functional integrity very sign

Language: Английский

Citations

2