Adult hippocampal neurogenesis: an important target associated with antidepressant effects of exercise

2017 ◽  
Vol 28 (7) ◽  
pp. 693-703 ◽  
Author(s):  
Lina Sun ◽  
Qingshan Sun ◽  
Jinshun Qi
Keyword(s):  
Adult Neurogenesis ◽  
Healthy Lifestyle ◽  
Brain Plasticity ◽  
Treatment Method ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Brain Functions ◽  
Antidepressant Effects ◽  
Exercise Activity ◽  
The Brain

AbstractDepression is a prevalent devastating mental disorder that affects the normal life of patients and brings a heavy burden to whole society. Although many efforts have been made to attenuate depressive/anxiety symptoms, the current clinic antidepressants have limited effects. Scientists have long been making attempts to find some new strategies that can be applied as the alternative antidepressant therapy. Exercise, a widely recognized healthy lifestyle, has been suggested as a therapy that can relieve psychiatric stress. However, how exercise improves the brain functions and reaches the antidepressant target needs systematic summarization due to the complexity and heterogeneous feature of depression. Brain plasticity, especially adult neurogenesis in the hippocampus, is an important neurophysiology to facilitate animals for neurogenesis can occur in not only humans. Many studies indicated that an appropriate level of exercise can promote neurogenesis in the adult brains. In this article, we provide information about the antidepressant effects of exercise and its implications in adult neurogenesis. From the neurogenesis perspective, we summarize evidence about the effects of exercise in enhancing neurogenesis in the hippocampus through regulating growth factors, neurotrophins, neurotransmitters and metabolism as well as inflammations. Taken together, a large number of published works indicate the multiple benefits of exercise in the brain functions of animals, particularly brain plasticity like neurogenesis and synaptogenesis. Therefore, a new treatment method for depression therapy can be developed by regulating the exercise activity.

scholarly journals Role of Adiponectin in Central Nervous System Disorders

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Jenna Bloemer ◽  
Priyanka D. Pinky ◽  
Manoj Govindarajulu ◽  
Hao Hong ◽  
Robert Judd ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Energy Homeostasis ◽  
Peripheral Circulation ◽  
Hippocampal Neurogenesis ◽  
Cns Disorders ◽  
Brain Functions ◽  
Glucose And Lipid Metabolism ◽  
Antidepressant Effects ◽  
The Brain

Adiponectin, the most abundant plasma adipokine, plays an important role in the regulation of glucose and lipid metabolism. Adiponectin also possesses insulin-sensitizing, anti-inflammatory, angiogenic, and vasodilatory properties which may influence central nervous system (CNS) disorders. Although initially not thought to cross the blood-brain barrier, adiponectin enters the brain through peripheral circulation. In the brain, adiponectin signaling through its receptors, AdipoR1 and AdipoR2, directly influences important brain functions such as energy homeostasis, hippocampal neurogenesis, and synaptic plasticity. Overall, based on its central and peripheral actions, recent evidence indicates that adiponectin has neuroprotective, antiatherogenic, and antidepressant effects. However, these findings are not without controversy as human observational studies report differing correlations between plasma adiponectin levels and incidence of CNS disorders. Despite these controversies, adiponectin is gaining attention as a potential therapeutic target for diverse CNS disorders, such as stroke, Alzheimer’s disease, anxiety, and depression. Evidence regarding the emerging role for adiponectin in these disorders is discussed in the current review.

scholarly journals Agrin-Lrp4-Ror2 signaling regulates adult hippocampal neurogenesis in mice

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Hongsheng Zhang ◽  
Anupama Sathyamurthy ◽  
Fang Liu ◽  
Lei Li ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Orphan Receptor ◽  
Brain Functions ◽  
Density Lipoprotein Receptor ◽  
Neural Stem Progenitor Cells ◽  
Newborn Neurons

Adult neurogenesis in the hippocampus may represent a form of plasticity in brain functions including mood, learning and memory. However, mechanisms underlying neural stem/progenitor cells (NSPCs) proliferation are not well understood. We found that Agrin, a factor critical for neuromuscular junction formation, is elevated in the hippocampus of mice that are stimulated by enriched environment (EE). Genetic deletion of the Agrn gene in excitatory neurons decreases NSPCs proliferation and increases depressive-like behavior. Low-density lipoprotein receptor-related protein 4 (Lrp4), a receptor for Agrin, is expressed in hippocampal NSPCs and its mutation blocked basal as well as EE-induced NSPCs proliferation and maturation of newborn neurons. Finally, we show that Lrp4 interacts with and activates receptor tyrosine kinase-like orphan receptor 2 (Ror2); and Ror2 mutation impairs NSPCs proliferation. Together, these observations identify a role of Agrin-Lrp4-Ror2 signaling for adult neurogenesis, uncovering previously unexpected functions of Agrin and Lrp4 in the brain.

Investigating the role of the ghrelin axis in cognitive decline and dementia

2021 ◽  
Author(s):  
◽  
Martina Sassi
Keyword(s):  
Mouse Model ◽  
Cognitive Decline ◽  
Young Animal ◽  
Active Form ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Tg2576 Mouse ◽  
Brain Functions ◽  
Acyl Ghrelin ◽  
The Brain

Ghrelin is a 28-amino acid hormone that is generated in a wide number of tissues. Its active form, acyl-ghrelin is able to bind to its receptor GHS-R and exert a variety of functions. In the brain, acyl-ghrelin has been associated with neuroprotection, improved memory and adult hippocampal neurogenesis (AHN). However, the mechanisms controlling acyl-ghrelin-mediated AHN are still unknown. To elucidate this process, different markers of neurogenesis were assessed in a mouse model in which GHS-R+ neurones were ablated specifically from the rostral DG of the hippocampus (rDG), showing that rDG GHS-R+ neurones are essential for maintaining AHN. Acyl-ghrelin has also been shown to prevents the damage caused by neurodegeneration, at least in young animal models of disease. In this thesis, we demonstrated that in the geriatric Tg2576 mouse model of Alzheimer’s disease, acyl-ghrelin maintained an effect on β-amyloid (Aβ) plaques in the hippocampus, promoting a reduction of the Aβ plaques size in AD-like mouse model compared to WT mice. Collectively, research findings highlight the importance of circulating acyl-ghrelin in the brain. However, ghrelin exists in two distinct forms and acyl-ghrelin can be enzymatically modified to the ‘inactive' unacylated-ghrelin (UAG) by acyl-protein thioesterase 1 (APT1). Preventing APT1 mediated de-acylation and increasing acyl-ghrelin bio-availability may prevent the damage caused by neurodegeneration. Unpublished data from our group suggest that PalmostatinB, an APT1 inhibitor, increases levels of acyl-ghrelin in macrophage cells (that naturally produce ghrelin). Therefore, this and other APT1 inhibitors may be considered possible therapeutic agents for the treatment of cognitive decline and diseases associated with dementia. We confirmed that, among several APT1 inhibitors, PalmostatinB is able to increase the level of acyl-ghrelin in vitro. However, further research is warranted into APT1 inhibitors as a novel therapeutic approach to treating cognitive decline and dementia. Together, the data in this thesis support a role for the ghrelinergic system components in modulating brain functions.

scholarly journals A Common Language: How Neuroimmunological Cross Talk Regulates Adult Hippocampal Neurogenesis

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Odette Leiter ◽  
Gerd Kempermann ◽  
Tara L. Walker
Keyword(s):  
Immune System ◽  
Adult Neurogenesis ◽  
Immune Cells ◽  
Hippocampal Neurogenesis ◽  
Adult Brain ◽  
Adult Hippocampal Neurogenesis ◽  
Normal Brain ◽  
Intrinsic Cues ◽  
Normal Brain Function ◽  
The Brain

Immune regulation of the brain is generally studied in the context of injury or disease. Less is known about how the immune system regulates the brain during normal brain function. Recent work has redefined the field of neuroimmunology and, as long as their recruitment and activation are well regulated, immune cells are now known to have protective properties within the central nervous system in maintaining brain health. Adult neurogenesis, the process of new neuron generation in the adult brain, is highly plastic and regulated by diverse extrinsic and intrinsic cues. Emerging research has shown that immune cells and their secreted factors can influence adult neurogenesis, both under baseline conditions and during conditions known to change neurogenesis levels, such as aging and learning in an enriched environment. This review will discuss how, under nonpathological conditions, the immune system can interact with the neural stem cells to regulate adult neurogenesis with particular focus on the hippocampus—a region crucial for learning and memory.

scholarly journals Polyphenol-rich extract from grape and blueberry attenuates cognitive decline and improves neuronal function in aged mice

2018 ◽  
Vol 7 ◽  
Author(s):  
Julien Bensalem ◽  
Stéphanie Dudonné ◽  
David Gaudout ◽  
Laure Servant ◽  
Frédéric Calon ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Learning And Memory ◽  
High Performance ◽  
Brain Plasticity ◽  
Memory Deficits ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Native Form ◽  
Age Related ◽  
The Brain

AbstractAgeing is characterised by memory deficits, associated with brain plasticity impairment. Polyphenols from berries, such as flavan-3-ols, anthocyanins, and resveratrol, have been suggested to modulate synaptic plasticity and cognitive processes. In the present study we assessed the preventive effect of a polyphenol-rich extract from grape and blueberry (PEGB), with high concentrations of flavonoids, on age-related cognitive decline in mice. Adult and aged (6 weeks and 16 months) mice were fed a PEGB-enriched diet for 14 weeks. Learning and memory were assessed using the novel object recognition and Morris water maze tasks. Brain polyphenol content was evaluated with ultra-high-performance LC-MS/MS. Hippocampal neurotrophin expression was measured using quantitative real-time PCR. Finally, the effect of PEGB on adult hippocampal neurogenesis was assessed by immunochemistry, counting the number of cells expressing doublecortin and the proportion of cells with dendritic prolongations. The combination of grape and blueberry polyphenols prevented age-induced learning and memory deficits. Moreover, it increased hippocampal nerve growth factor (Ngf) mRNA expression. Aged supplemented mice displayed a greater proportion of newly generated neurons with prolongations than control age-matched mice. Some of the polyphenols included in the extract were detected in the brain in the native form or as metabolites. Aged supplemented mice also displayed a better survival rate. These data suggest that PEGB may prevent age-induced cognitive decline. Possible mechanisms of action include a modulation of brain plasticity. Post-treatment detection of phenolic compounds in the brain suggests that polyphenols may act directly at the central level, while they can make an impact on mouse survival through a potential systemic effect.

scholarly journals Stress-Related Dysfunction of Adult Hippocampal Neurogenesis—An Attempt for Understanding Resilience?

2021 ◽  
Vol 22 (14) ◽  
pp. 7339
Author(s):  
Julia Leschik ◽  
Beat Lutz ◽  
Antonietta Gentile
Keyword(s):  
Major Depression ◽  
Adult Neurogenesis ◽  
Current Knowledge ◽  
Functional Relation ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Special Focus ◽  
Extrinsic Cues ◽  
Health And Disease ◽  
Newborn Neurons

Newborn neurons in the adult hippocampus are regulated by many intrinsic and extrinsic cues. It is well accepted that elevated glucocorticoid levels lead to downregulation of adult neurogenesis, which this review discusses as one reason why psychiatric diseases, such as major depression, develop after long-term stress exposure. In reverse, adult neurogenesis has been suggested to protect against stress-induced major depression, and hence, could serve as a resilience mechanism. In this review, we will summarize current knowledge about the functional relation of adult neurogenesis and stress in health and disease. A special focus will lie on the mechanisms underlying the cascades of events from prolonged high glucocorticoid concentrations to reduced numbers of newborn neurons. In addition to neurotransmitter and neurotrophic factor dysregulation, these mechanisms include immunomodulatory pathways, as well as microbiota changes influencing the gut-brain axis. Finally, we discuss recent findings delineating the role of adult neurogenesis in stress resilience.

Potential Role of Adult Hippocampal Neurogenesis in Traumatic Brain Injury

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Cognitive Outcomes ◽  
Adult Hippocampal Neurogenesis ◽  
The Brain

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.

scholarly journals Does Impairment of Adult Neurogenesis Contribute to Pathophysiology of Alzheimer's Disease? A Still Open Question

2021 ◽  
Vol 13 ◽  
Author(s):  
Domenica Donatella Li Puma ◽  
Roberto Piacentini ◽  
Claudio Grassi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Adult Neurogenesis ◽  
Memory Formation ◽  
Hippocampal Neurogenesis ◽  
Synaptic Function ◽  
Adult Hippocampal Neurogenesis ◽  
Amyloid Β Protein

Adult hippocampal neurogenesis is a physiological mechanism contributing to hippocampal memory formation. Several studies associated altered hippocampal neurogenesis with aging and Alzheimer's disease (AD). However, whether amyloid-β protein (Aβ)/tau accumulation impairs adult hippocampal neurogenesis and, consequently, the hippocampal circuitry, involved in memory formation, or altered neurogenesis is an epiphenomenon of AD neuropathology contributing negligibly to the AD phenotype, is, especially in humans, still debated. The detrimental effects of Aβ/tau on synaptic function and neuronal viability have been clearly addressed both in in vitro and in vivo experimental models. Until some years ago, studies carried out on in vitro models investigating the action of Aβ/tau on proliferation and differentiation of hippocampal neural stem cells led to contrasting results, mainly due to discrepancies arising from different experimental conditions (e.g., different cellular/animal models, different Aβ and/or tau isoforms, concentrations, and/or aggregation profiles). To date, studies investigating in situ adult hippocampal neurogenesis indicate severe impairment in most of transgenic AD mice; this impairment precedes by several months cognitive dysfunction. Using experimental tools, which only became available in the last few years, research in humans indicated that hippocampal neurogenesis is altered in cognitive declined individuals affected by either mild cognitive impairment or AD as well as in normal cognitive elderly with a significant inverse relationship between the number of newly formed neurons and cognitive impairment. However, despite that such information is available, the question whether impaired neurogenesis contributes to AD pathogenesis or is a mere consequence of Aβ/pTau accumulation is not definitively answered. Herein, we attempted to shed light on this complex and very intriguing topic by reviewing relevant literature on impairment of adult neurogenesis in mouse models of AD and in AD patients analyzing the temporal relationship between the occurrence of altered neurogenesis and the appearance of AD hallmarks and cognitive dysfunctions.

FC29-02 - Is prenatal exposure to alcohol a factor which re-program the brain?

2011 ◽  
Vol 26 (S2) ◽  
pp. 1978-1978
Author(s):  
J.H. Sliwowska
Keyword(s):  
Prenatal Exposure ◽  
Hpa Axis ◽  
Alcohol Exposure ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Ovariectomized Rats ◽  
List Type ◽  
Depression And Anxiety ◽  
Hpg Axis ◽  
The Brain

IntroductionFetal programming refers to the concept that early environmental factors, including prenatal exposure to stress and drugs, can permanently organize or imprint physiological and behavioural systems and increase vulnerability to disorders such as depression and anxiety later in life.AimsIs prenatal exposure to alcohol a factor which re-programs the brain?ObjectivesEffects of prenatal alcohol exposure (PAE) on:1)the hypothalamus-pituitary-adrenal (HPA) axis;2)the hypothalamus-pituitary-gonadal (HPG) axis;3)serotonergic (5-HT) system and4)adult hippocampal neurogenesis are presented.MethodsOffspring from prenatal ethanol (PAE), pair-fed (PF) and ad lib-fed control (C) dams are studied across the development or in adulthood. Immunocytochemistry and in situ hybridization techniques are used.ResultsIn term of the HPA axis: PAE alters the balance of mineralocorticoids/glucocorticoids (MRs/GRs) receptor levels in the hippocampus of adult females. In the case of the HPG axis: PAE delays puberty and changes hormonal profiles in males and females. PAE also decreases numbers of 5-HT-immunoreactive neurons in the dorsal raphe nucleus of the brainstem in ovariectomized rats and estradiol and progesterone modulate those effects. Finally, in adult PAE males, but not females stress-induced decrease in neurogenesis is altered.ConclusionsIn our animal model PAE re-programs the brain. Effects of PAE are long-lasting, affect HPA and HPG axes, 5-HT system and adult hippocampal neurogenesis and if seen in humans could contribute to increased vulnerability to depression and anxiety.

EYE ON CHINA

2017 ◽  
Vol 21 (08) ◽  
pp. 4-12
Keyword(s):  
Breast Cancer ◽  
Initial Public Offering ◽  
Memory Formation ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Technological Innovations ◽  
Cooperation Agreement ◽  
Diagnose Breast Cancer ◽  
Public Offering ◽  
The Brain

Palm-Sized PCR Device for Rapid Real-Time Detection of Viruses. Scientists Uncover New Mechanism for Diabetic Neuropathy. Chi Med Initiates a Phase I/II Clinical Trial of Novel FGFR Inhibitor HMPL 453 in China. Database Boosts Shanghai’s Technology Aim. Experts Emphasize Scientific and Technological Innovations in Agriculture. China Enlists AI to Diagnose Breast Cancer. Study Offers Clue to Memory Formation in the Brain. China Signed Science Cooperation Agreement with Bolivia. Biotechnology in China Hits 4 Trillion RMB in 2016. A Novel Pathway: Adult Hippocampal Neurogenesis Linked to Depression Caused by Inflammation. BGI Genomics Announces Pricing of Initial Public Offering.

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