IFIP advances in information and communication technology, Journal Year: 2024, Volume and Issue: unknown, P. 79 - 90
Published: Jan. 1, 2024
Language: Английский
IFIP advances in information and communication technology, Journal Year: 2024, Volume and Issue: unknown, P. 79 - 90
Published: Jan. 1, 2024
Language: Английский
Pharmacology Biochemistry and Behavior, Journal Year: 2022, Volume and Issue: 215, P. 173371 - 173371
Published: March 8, 2022
Language: Английский
Citations
17Cells, Journal Year: 2022, Volume and Issue: 11(16), P. 2603 - 2603
Published: Aug. 21, 2022
Behavioural and psychological symptoms of dementia (BPSD) are presented in 95% Alzheimer’s Disease (AD) patients also associated with neurotrophin deficits. The molecular mechanisms leading to age-related diseases still unclear; however, emerging evidence has suggested that epigenetic modulation is a key pathophysiological basis ageing neurodegeneration. In particular, it been G9a methyltransferase its repressive histone mark (H3K9me2) important shaping learning memory by modulating autophagic activity synaptic plasticity. This work deepens our understanding the underlying loss cognitive function BPSD AD. For this purpose, several tasks were performed evaluate parameters sociability (three-chamber test), aggressiveness (resident intruder), anxiety (elevated plus maze open field) (novel object recognition test) mice, followed evaluation epigenetic, autophagy plasticity markers at level. behavioural alterations senescence-accelerated mice prone 8 (SAMP8) 12 months age compared their mouse resistant (SAMR1), healthy control strain was accompanied deficits markers. Increased levels concomitant dysregulation JNK pathway aged SAMP8, driving failure autophagosome formation. Furthermore, lower expression genes involved memory-consolidation process modulated ERK observed male SAMP8 model, suggesting implication G9a. any case, two most neurotrophins, namely brain-derived neurotrophic factor (Bdnf) neurotrophin-3 (NT3), found be reduced, along decrease dendritic branching spine density mice. Thus, present study characterizes provides information regarding non-cognitive states, as well alterations, demonstrating AD-like model. results indicate higher plasticity, which could further explain decline exhibited
Language: Английский
Citations
17Pharmacological Reports, Journal Year: 2020, Volume and Issue: 73(2), P. 346 - 356
Published: Dec. 31, 2020
Depression is currently one of the most common psychiatric disorders and number patients receiving antidepressant treatment increasing every year. Therefore, it essential to understand underlying mechanisms that are associated with higher prevalence depression. The main component leading change in functioning, form apathy, anhedonia, lack motivation sleep disturbances, stress. This factor recent decades-due civilization speed, dynamic technological development as well competitiveness competition relationships-significantly affects psychophysical condition, which results an increase diseases, including To mechanism susceptibility this disease, should consider significant role interaction between immune nervous systems. Their joint from moment conception a matrix later predispositions, both mobilization proinflammatory pathways (TNFα, IL-1β, IL-6) psychological coping Such early period epigenetic processes strongly marked prenatal up 1 year age determinate characteristic phenotype for various forms pathology, Regarding inflammatory hypothesis depression, interleukin 17 (IL-17), among other cytokines, might play important depressive disorders. It secreted by Th17 cells, crossed placental barrier acts on brain structures fetus IL-17 receptor levels affecting intensity its signaling brain.
Language: Английский
Citations
26Journal of Affective Disorders, Journal Year: 2020, Volume and Issue: 276, P. 850 - 858
Published: July 22, 2020
Language: Английский
Citations
25IFIP advances in information and communication technology, Journal Year: 2024, Volume and Issue: unknown, P. 79 - 90
Published: Jan. 1, 2024
Language: Английский
Citations
3