Functional Role of Physical Exercise and Omega-3 Fatty Acids on Depression and Mood Disorders

Farioli-Vecchioli, Stefano; Cutuli, Debora

doi:10.1007/978-3-031-24930-3_12

Cited by 1 publication

(1 citation statement)

References 286 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, the latency of antidepressant efficacy is comparable to the time required for fully maturation and differentiation of newly formed neurons. Moreover, there are several lines of evidence that support the neurogenesis hypothesis such as the reduction of hippocampal neurogenesis upon stress, increasing hippocampal neurogenesis after antidepressant, and the complete elimination of antidepressant effect upon ablation of hippocampal neurogenesis (Farioli‐Vecchioli & Cutuli, 2023) Thus, this new hypothesis may be valid an alternate to monoamine hypothesis. Altering neurogenesis levels can significantly impact anxiety, with a decrease tending to exacerbate it, while an increase can have anxiolytic and antidepressant effects.…”

Section: β‐Catenin and Neurogenesis In Psychiatric Disordersmentioning

confidence: 97%

Influence of β‐catenin signaling on neurogenesis in neuropsychiatric disorders: Anxiety and depression

El‐Kadi,

AbdelKader,

Zaki

et al. 2024

Drug Development Research

View full text Add to dashboard Cite

It has been proven that stress, mainly in the early years of life, can lead to anxiety and mood problems. Current treatments for psychiatric disorders are not enough, and some of them show intolerable side effects, emphasizing the urgent need for new treatment targets. Hence, a better understanding of the different brain networks, which are involved in the response to anxiety and depression, may evoke treatments with more specific targets. One of these targets is β‐catenin that regulates brain circuits. β‐Catenin has a dual response toward stress, which may influence coping or vulnerability to stress response. Indeed, β‐catenin signaling involves several processes such as inflammation‐directed brain repair, inflammation‐induced brain damage, and neurogenesis. Interestingly, β‐catenin reduction is accompanied by low neurogenesis, which leads to anxiety and depression. However, in another state, this reduction activates a compensatory mechanism that enhances neurogenesis to protect against depression but may precipitate anxiety. Thus, understanding the molecular mechanism of β‐catenin could enhance our knowledge about anxiety and depression's pathophysiology, potentially improving clinical results by targeting it. Herein, the different states of β‐catenin were discussed, shedding light on possible drugs that showed action on psychiatric disorders through β‐catenin.

show abstract

Section: β‐Catenin and Neurogenesis In Psychiatric Disordersmentioning

confidence: 97%