Noopept Reduces the Postischemic Functional and Metabolic Disorders in the Brain of Rats with Different Sensitivity to Hypoxia

2009 ◽  
Vol 147 (3) ◽  
pp. 339-344 ◽  
Author(s):  
I. V. Zarubina ◽  
P. D. Shabanov
Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 940
Author(s):  
Li Wu ◽  
Yuqiu Han ◽  
Zhipeng Zheng ◽  
Shuai Zhu ◽  
Jun Chen ◽  
...  

Anxiety is one of the complications of metabolic disorders (MDs). Obeticholic acid (OCA), the bile acids (BAs) derivative, is a promising agent for improving MDs in association with gut dysbiosis. Yet, its protective effect on MDs-driven anxiety remains unknown. Here, we assessed the serum biochemical parameters and behavioral performance by open field and Morris water maze tests in HFHS diet-induced MDs mice after OCA intervention for nine and 18 weeks. Moreover, antibiotics intervention for microbial depletion was conducted simultaneously. We found that OCA treatment inhibited the initiation and progression of anxiety in HFHS diet-MDs mice via a microbiota–BAs–brain axis: OCA decreased the neuroinflammatory microglia and IL-1β expression in the hippocampus, reversed intestinal barrier dysfunction and serum proinflammatory LPS to a normal level, modified the microbial community, including the known anxiety-related Rikenellaceae and Alistipes, and improved the microbial metabolites especially the increased BAs in feces and circulation. Moreover, the OCA-reversed bile acid taurocholate linked disordered serum lipid metabolites and indole derivatives to anxiety as assessed by network analysis. Additionally, microbial depletion with antibiotics also improved the anxiety, microgliosis and BAs enrichment in the experimental MDs mice. Together, these findings provide microbiota–BAs–brain axis as a novel therapeutic target for MDs-associated neuropsychiatric disorders.


INDIAN DRUGS ◽  
2013 ◽  
Vol 50 (01) ◽  
pp. 5-22
Author(s):  
K Challabotla ◽  
◽  
D Banji ◽  
O.J.F Banji ◽  
Chilipi K Reddy

Ageing is a natural process characterized by progressive deterioration of biological functions. Ageing causes both morphological as well as biochemical alterations in various body organs leading to deterioration of health. Proteins, enzymes and neurotransmitters are affected, which in turn can result in dysregulation of various pathways. WHO has reported that by 2020, three quarters of all deaths in developing countries will be age-associated. Currently more than 300 theories exist to explain the phenomenon of ageing; amongst them the oxidative stress theory of ageing is most studied and accepted for the molecular basis of ageing. All these processes can progress at an unprecedented pace on contact with triggering factors, leading to the development of pathological ageing. The probability of developing neurodegenerative and metabolic disorders is relatively high under such circumstances. This review emphasizes the theories and mechanisms of ageing and an overview on the aspects of age associated biochemical changes and the implications on the brain, liver and various organ systems.


2020 ◽  
Vol 98 (10) ◽  
pp. 1889-1904 ◽  
Author(s):  
Ali Shahandeh ◽  
Bang V. Bui ◽  
David I. Finkelstein ◽  
Christine T. O. Nguyen

2011 ◽  
Vol 32 (6) ◽  
pp. 615-636 ◽  
Author(s):  
Sangam Kanekar ◽  
Joel Verbrugge

2018 ◽  
Vol 2 (1) ◽  
pp. 01-03
Author(s):  
Navya K

Adrenal Gland The adrenal glands are controlled in part by the brain. The hypothalamus, a small area of the brain involved in hormonal regulation, produces corticotropin-releasing hormone (CRH) and vasopressin (also known as antidiuretic hormone). Vasopressin and CRH trigger the pituitary gland to secrete corticotropin (also known as adrenocorticotropic hormone or ACTH), which stimulates the adrenal glands to produce corticosteroids. The renin-angiotensin-aldosterone system, regulated mostly by the kidneys, causes the adrenal glands to produce more or less aldosterone. The body controls the levels of corticosteroids according to need. The levels tend to be much higher in the early morning than later in the day. When the body is stressed, due to illness or otherwise, the levels of corticosteroids increase dramatically.


Author(s):  
Sapna Singh ◽  
Veena Chowdhury

1996 ◽  
Vol 17 (8) ◽  
pp. 265-278
Author(s):  
Michael J. Rivkin ◽  
Joseph J. Volpe

Stroke denotes the sudden onset of a focal neurologic deficit and most often includes the abrupt appearance of weakness. Interruption of blood flow to a part of the central nervous system (CNS) usually underlies the resultant weakness. Because most strokes in children are related to focal cerebral involvement, the most common clinical manifestation is the abrupt appearance of hemiparesis. Less frequently, the cause of stroke involves the brain stem, cerebellum, or spinal cord. The functional consequences always reflect the neuroanatomic features of the affected CNS region. Epidemiology Childhood stroke occurs with an annual incidence of 2.5 cases per 100,000 population and has been reported in all racial and ethnic groups. The sequelae are not trivial. In addition to lasting lateralized weakness, cognitive deficits, disturbances of language, visual deficits, and seizures may persist long after the acute event has concluded. The causes of stroke in children differ from those in adults. Stroke in adults is associated largely with hypertension or atherosclerosis and their respective hemorrhagic and ischemic consequences. Stroke in children more commonly is caused by or related to congenital heart disease, infection, metabolic disorders, hematologic diatheses, and vasculitic disorders, frequently due to autoimmune processes (Table 1). Nonetheless, despite the most thorough of evaluations, etiology escapes detection in approximately 30% of the pediatric patients in whom stroke occurs.


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