Metabolic Brain Disease, Год журнала: 2024, Номер 40(1)
Опубликована: Дек. 13, 2024
Язык: Английский
Pharmacological Research, Год журнала: 2025, Номер unknown, С. 107615 - 107615
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
3
Molecular and Cellular Biochemistry, Год журнала: 2025, Номер unknown
Опубликована: Фев. 12, 2025
Язык: Английский
Процитировано
2
Immunity & Ageing, Год журнала: 2025, Номер 22(1)
Опубликована: Янв. 3, 2025
Obesity and metabolic syndrome are major public health concerns linked to cognitive decline with aging. Prior work from our lab has demonstrated that short-term high fat diet (HFD) rapidly impairs memory function via a neuroinflammatory mechanism. However, the degree which these rapid inflammatory changes unique brain is unknown. Moreover, deviations in gut microbiome composition have been associated obesity impairment, but how aging interact impact microbiome, or occur, less clear. Thus, study investigated of HFD after two distinct consumption durations: 3 months (to model diet-induced obesity) days detect occurring HFD) on function, anxiety-like behavior, central peripheral inflammation, profile young aged rats.
Язык: Английский
Процитировано
0
Behavioural Brain Research, Год журнала: 2025, Номер unknown, С. 115510 - 115510
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0
Biomedicines, Год журнала: 2024, Номер 12(8), С. 1716 - 1716
Опубликована: Авг. 1, 2024
The term 'inflammaging' has been coined to describe the chronic state of inflammation derived from ongoing cycles tissue damage and subsequent immune responses. This inflammatory status contributes decline organs physiological functions, accelerates aging process, increases risk age-related illnesses death. During aging, gut microbiota (GM) undergoes significant changes, including a decreased diversity species, in beneficial bacteria, rise proinflammatory ones, resulting persistent low-grade inflammation. Moreover, environmental factors, such as diet medications, contribute changes GM function, preventing or promoting inflammaging. narrative review aims clarify underlying mechanisms inflammaging specifically investigate influence several factors on these mechanisms, while also exploring potential differences related sex. lifestyle pharmacological interventions will be suggested promote healthy aging.
Язык: Английский
Процитировано
2
Neuropharmacology, Год журнала: 2024, Номер 259, С. 110108 - 110108
Опубликована: Авг. 10, 2024
Consumption of saturated fat-enriched diets during adolescence has been closely associated with the reduction hippocampal synaptic plasticity and impairment cognitive function. Nevertheless, effect long-term intake these foods not yet studied. In present study, we have investigated a treatment, lasting for 40 weeks, diet enriched in fat (SOLF) on i) spatial learning memory, ii) transmission plasticity, iii) gene expression levels aged male female mice. Our findings reveal that SOLF detrimental impact memory mechanisms, such as potentiation (LTP), downregulates Gria1 specifically males. females, Gria1/2/3 Grin1/2A/2B glutamate receptor subunits well some proinflammatory interleukins. These highlight importance considering sex-specific factors when assessing effects high-fat cognition brain plasticity.
Язык: Английский
Процитировано
2
Neurochemical Research, Год журнала: 2024, Номер unknown
Опубликована: Сен. 20, 2024
Язык: Английский
Процитировано
1
Gut Microbes, Год журнала: 2024, Номер 16(1)
Опубликована: Окт. 16, 2024
High-fat diet (HFD) has been linked to female infertility. However, the specific age at which HFD impacts ovarian function and underlying mechanisms remain poorly understood. Here, we administered a mice various developmental stages: pre-puberty (4 weeks old), post-puberty (6 young adult (9 middle (32 old). Our observations indicated that was most significantly compromised when initiated post-puberty. Consequently, were chosen for further investigation. Through transplantation of fecal bacteria from on normal diet, confirmed gut microbiota dysbiosis contributed HFD-induced deteriorated fertility disrupted estradiol synthesis. Utilizing untargeted targeted metabolomics analyses, identified L-saccharopine as key metabolite, enriched in feces, serum, ovaries HFD-FMT mice. Subsequent
Язык: Английский
Процитировано
1
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(23), С. 12637 - 12637
Опубликована: Ноя. 25, 2024
Neurodegeneration is preeminent in many neurological diseases, and still a major burden we fail to manage patient's care. Its pathogenesis complicated, intricate, far from being completely understood. Taking multiple sclerosis as an example, propose that neurodegeneration neither cause nor consequence by itself. Mitochondrial dysfunction, leading energy deficiency ion imbalance, plays key role neurodegeneration, partly caused the oxidative stress generated microglia astrocytes. Nodal paranodal disruption, with or without myelin alteration, further involved. Myelin loss exposes axons directly inflammatory environment. Moreover, oligodendrocytes provide singular metabolic trophic support axons, but do not emerge unscathed pathological events, primary defects cell apoptosis secondary neuroinflammation axonal damage. Hereby, failure might be overlooked contributor neurodegeneration. Thus, complex interplay between neuroinflammation, demyelination, wherein each primarily secondarily involved, offer more comprehensive understanding of help establishing novel therapeutic strategies for diseases beyond.
Язык: Английский
Процитировано
1
Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)
Опубликована: Дек. 18, 2024
Abstract Norepinephrine (NE) modulates cognitive function, arousal, attention, and responses to novelty stress, it also regulates neuroinflammation. We previously demonstrated behavioral immunomodulatory effects of beta-adrenergic pharmacology in mouse models Alzheimer’s disease (AD). The current studies were designed block noradrenergic signaling 5XFAD mice through ( 1 ) chemogenetic inhibition the locus coeruleus (LC), 2 pharmacologic blocking β-adrenergic receptors, 3 conditional deletion β1- or β2-adrenergic receptors (adrb1 adrb2) microglia. First, brain-wide AD pathology was mapped 3D by imaging immunolabeled, cleared brains assess overlap between amyloid beta (Aβ) pathology, reactive microglia, loss tyrosine hydroxylase (TH) expression catecholaminergic system. To examine inhibiting LC NE system model, inhibitory (Gi) DREADD expressed specifically neurons. neurons chronically inhibited subcutaneous pump administration agonist clozapine-N-oxide (CNO). Plasma collected for assessment neuroinflammation pathology. A separate cohort dosed with antagonist propranolol vehicle evaluated behavior, as well post-mortem Finally, we used either adrb1 adrb2 microglia mediated signaling. Using iDISCO+, light sheet fluorescence microscopy, novel analyses, detected widespread microgliosis Aβ along modest TH downregulation fibers across multiple brain regions, contrast spatially limited observed Both adrenergic pharmacological potentiated without altering Conditional did not affect attenuated inflammation females but had no effect males. Overall, these data support previous observations demonstrating pathophysiology disorders suggest that on cell types other than such astrocytes, may mediate some disease-modifying agonists brain.
Язык: Английский
Процитировано
1