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V

V. Sterlemann

Researcher at Max Planck Society

Publications -  18
Citations -  1027

V. Sterlemann is an academic researcher from Max Planck Society. The author has contributed to research in topics: Social stress & Chronic stress. The author has an hindex of 13, co-authored 16 publications receiving 936 citations.

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Persistent neuroendocrine and behavioral effects of a novel, etiologically relevant mouse paradigm for chronic social stress during adolescence.

TL;DR: A novel chronic social stress paradigm in male mice during adolescence results in persistent alterations of hypothalamus-pituitary-adrenal axis function and behavior, which are reversible by pharmacological treatment and allows to investigate the interaction of genetic susceptibility and environmental risk factors.
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Long-term behavioral and neuroendocrine alterations following chronic social stress in mice: Implications for stress-related disorders

TL;DR: It is demonstrated that chronic stress exposure during a crucial developmental time period results in long-term, persistent effects on physiological and behavioral parameters throughout life, which may contribute to an enhanced vulnerability to stress-induced diseases.
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Chronic Social Stress During Adolescence Induces Cognitive Impairment in Aged Mice

TL;DR: The results identify possible molecular mechanisms underlying cognitive impairment during aging, demonstrating the detrimental impact of stress during adolescence on hippocampus‐dependent cognitive function in aged mice.
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High susceptibility to chronic social stress is associated with a depression-like phenotype.

TL;DR: It is shown that by using a large cohort of animals it is possible to select individuals that are vulnerable or resilient to the lasting effects of chronic social stress, and the vulnerable phenotype mimics many aspects of stress-related human affective disorders.
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Metabolic Signals Modulate Hypothalamic‐Pituitary‐Adrenal Axis Activation During Maternal Separation of the Neonatal Mouse

TL;DR: It is suggested that metabolic signals play an important role in triggering the HPA response of the neonate to maternal separation, and prevention of reduction in blood glucose or blockade of the ghrelin signalling pathway is recommended.