Homocysteine Mediates Cognitive Inflexibility Induced by Stress via Targeting PIN1

Brain Sciences, Год журнала: 2025, Номер 15(4), С. 416 - 416

Опубликована: Апрель 19, 2025

Background: Increasing evidence shows that HCY plays an important role in stress-induced cognitive dysfunction, and significantly promotes the decline of function. Stress has been reported to cause elevated hippocampus mice. Cognitive flexibility refers ability individuals quickly adjust their neurobehavioral strategies different situations or solve tasks. Aims: This study aims explore impairment induced by stress its possible regulatory mechanism. Methods: First, we examined changes protein mRNA levels effector molecule, PIN1, during The results show can a mice lead increase PIN1. Moreover, through use vitro experiments, found could induce PIN1 expression neurons. Further vivo experiments were used investigate effect VitB on evaluated therapeutic flexibility. decreased plasma hippocampus, alleviated flexibility, reduced Conclusions: These suggest be inhibited regulating content HCY. Collectively, our findings highlight aimed at improving treatment for impairments

Язык: Английский

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The association of structural versus load-dependent large artery stiffness mechanisms with cerebrovascular damage and cortical atrophy in humans

GeroScience, Год журнала: 2024, Номер 46(6), С. 5587 - 5597

Опубликована: Июнь 20, 2024

Язык: Английский

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Androgen deprivation exacerbates AD pathology by promoting the loss of microglia in an age-dependent manner

Life Sciences, Год журнала: 2024, Номер 355, С. 122973 - 122973

Опубликована: Авг. 12, 2024

Язык: Английский

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CB1 Receptors In NG2 CELLS MEDIATE CANNABINOID-EVOKED FUNCTIONAL MYELIN REGENERATION

Progress in Neurobiology, Год журнала: 2024, Номер 243, С. 102683 - 102683

Опубликована: Ноя. 9, 2024

Язык: Английский

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Should We Consider Neurodegeneration by Itself or in a Triangulation with Neuroinflammation and Demyelination? The Example of Multiple Sclerosis and Beyond

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

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DNA damage and senescence in the aging and Alzheimer’s disease cortex are not uniformly distributed

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown

Опубликована: Апрель 30, 2024

ABSTRACT Alzheimer’s disease (AD) is a neurodegenerative illness with typical age of onset exceeding 65 years age. The age-dependency the condition led us to track appearance DNA damage in frontal cortex individuals who died diagnosis AD. focus on was motivated by evidence that increasing levels irreparable are major driver aging process. connection between and loss genomic integrity compelling because has also been identified as possible cause cellular senescence. number senescent cells reported increase age, their senescence-associated secreted products likely contributing factors age-related illnesses. We tracked 53BP1 senescence p16 immunostaining human post-mortem brain samples. found significantly increased BA9 region AD when compared same unaXected controls (UC). In but not UC cases, density distance from pia mater up approximately layer V then decreased deeper areas. This pattern overlaid senescence, which cortical depth. On cell-by-cell basis, we intensity two markers tightly linked AD, brain. To test whether causal factor emergence program, used etoposide treatment cultured mouse primary neurons. While after treatment, 24 hours no change expression observed. Our work suggests both increasingly coupled. propose vivo relationship processes more complex than previously thought.

Язык: Английский

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The mechanisms of white matter injury and immune system crosstalk in promoting the progression of Parkinson’s disease: a narrative review

Frontiers in Aging Neuroscience, Год журнала: 2024, Номер 16

Опубликована: Май 28, 2024

Parkinson’s disease (PD) is neurodegenerative in middle-aged and elderly people with some pathological mechanisms including immune disorder, neuroinflammation, white matter injury abnormal aggregation of alpha-synuclein, etc. New research suggests that may be important the development PD, but how inflammation, system, damage interact to harm dopamine neurons not yet understood. Therefore, it particularly delve into crosstalk between cells central peripheral nervous system based on study PD. This could only exacerbate process PD also reveal new therapeutic targets. By understanding penetrate through blood–brain barrier activate inflammatory responses within we can better grasp impact structural destruction explore this modulated mitigate or combat progression. Microglia, astrocytes, oligodendrocytes (especially T cells) play a role its where these produce respond pro-inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukin-1β(IL-1β) interleukin-6(IL-6), causes microglia become release mediators, which attract more damaged area, increasing response. Moreover, dysfunction barrier, allows factors invade brain further, enhances activation forming vicious circle intensifies neuroinflammation. And collectively promote neuroinflammatory environment neurodegeneration changes Overall, findings deepen our complexity provide targets for strategies focused inflammation regulation mechanisms. In summary, review provided theoretical basis clarifying pathogenesis summarized association systems, then emphasized their potential specific achieving further aggravating

Язык: Английский

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DNA Damage and Senescence in the Aging and Alzheimer’s Disease Cortex Are Not Uniformly Distributed

Biomedicines, Год журнала: 2024, Номер 12(6), С. 1327 - 1327

Опубликована: Июнь 14, 2024

Alzheimer’s disease (AD) is a neurodegenerative illness with typical age of onset exceeding 65 years age. The dependency the condition led us to track appearance DNA damage in frontal cortex individuals who died diagnosis AD. focus on was motivated by evidence that increasing levels irreparable are major driver aging process. connection between and loss genomic integrity compelling because has also been identified as possible cause cellular senescence. number senescent cells reported increase age, their senescence-associated secreted products likely contributing factors age-related illnesses. We tracked 53BP1 senescence p16 immunostaining human post-mortem brain samples. found significantly increased BA9 region AD compared same unaffected controls (UCs). In but not UC cases, density distance from pia mater up approximately layer V then decreased deeper areas. This pattern overlaid senescence, which cortical depth. On cell-by-cell basis, we intensities two markers were tightly linked brain. To test whether causal factor emergence program, used etoposide treatment cultured mouse primary neurons. While after treatment, 24 h, no change expression observed. Our work suggests both increasingly coupled. propose vivo, relationship processes more complex than previously thought.

Язык: Английский

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Exposed wires: A microbial metabolite influences myelination in the brain

Science, Год журнала: 2024, Номер 385(6704), С. 37 - 37

Опубликована: Июль 4, 2024

A microbial metabolite influences myelination in the brain.

Язык: Английский

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Als-Associated Tdp-43 Aggregates Drive Innate and Adaptive Immune Cell Activation

Опубликована: Янв. 1, 2024

Язык: Английский

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