Synapse formation on neurons born in the adult hippocampus

Toni, Nicolas; Teng, Edmond; Bushong, Eric A.; Aimone, James B.; Zhao, Chen; Consiglio, Antonella; Praag, Henriette van; Martone, Maryann E.; Ellisman, Mark H.; Gage, Fred H.

doi:10.1038/nn1908

Cited by 509 publications

(529 citation statements)

References 50 publications

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“…Imipramine and fluoxetine have been shown to increase both neuronal proliferation and survival in the adult hippocampus via activation of trkB/BDNF signaling: mice deficient in BDNF do not show enhanced neuronal survival after antidepressant treatment (Sairanen et al, 2005). Fluoxetine also promotes plasticity in the hippocampus by increasing pyramidal neuron dendritic spine density (Hajszan et al, 2005), which may provide a general enhancement of the synaptic input that new neurons require for survival and network integration (Kee et al, 2007;Toni et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Miller

Schultz

Gulati

et al. 2007

Neuropsychopharmacol

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Despite widespread use of antidepressants, the factors underlying the behavioral response to antidepressants are unknown. It has been shown that antidepressant treatment promotes the proliferation and survival of neurons in the adult hippocampus via enhanced serotonergic signaling, but it is unclear whether hippocampal neurogenesis is responsible for the behavioral response to antidepressants. Furthermore, a large subpopulation of patients fails to respond to antidepressant treatment due to presumed underlying genetic factors. In the present study, we have used the phenotypic and genotypic variability of inbred mouse strains to show that there is a genetic component to both the behavioral and neuronal effects of chronic fluoxetine treatment, and that this antidepressant induces an increase in hippocampal cell proliferation only in the strains that also show a positive behavioral response to treatment. Furthermore, the behavioral and neuronal responses are associated with an upregulation of genes known to promote neuronal proliferation and survival. These results suggest that inherent genetic predisposition to increased serotonin-induced neurogenesis may be a determinant of antidepressant efficacy.

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Section: Discussionmentioning

confidence: 99%

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Miller

Schultz

Gulati

et al. 2007

Neuropsychopharmacol

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“…these include precursors for membrane phosphatidylation such as uridine, choline and omega-3 polyunsaturated fatty acids (4)(5)(6). Reports have also indicated that combining these nutrients may improve cognition and increase hippocampal dendritic spines (7), again suggesting a positive effect on the formation of new synapses (8)(9)(10). it was therefore hypothesized that such agents may play a role in the management of ad.…”

mentioning

confidence: 99%

Efficacy of a medical food on cognition in Alzheimer's Disease: Results from secondary analyses of a randomized, controlled trial

Kamphuis

Verhey

Rikkert

et al. 2011

The Journal of nutrition, health and aging

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1. Nutricia advanced medical Nutrition, danone Research, centre for specialised Nutrition, Wageningen, the Netherlands; 2. utrecht institute for Pharmaceutical sciences (uiPs), utrecht university, the Netherlands; 3. alzheimer centre limburg, school for mental Health and Neuroscience, maastricht university medical centre, the Netherlands; 4. alzheimer centre Nijmegen, department of Geriatrics, Radboud university Nijmegen medical centre, the Netherlands; 5. department of Health sciences, Vu university medical center, amsterdam, the Netherlands; 6. alzheimer centre, Vu university medical center, amsterdam, the Netherlands. correspondence to: Professor Philip scheltens, department of Neurology and alzheimer center, Vu university medical center, de Boelelaan 1117, 1081 HV amsterdam, the Netherlands, p.scheltens@vumc.nl, tel: +31 (0) 20 444 0816, abstract: Objective: to investigate the extent that baseline cognitive impairment and intake adherence affected the 13-item alzheimer's disease assessment scale -cognitive subscale (adas-cog) intervention response of a medical food in alzheimer's disease (ad) patients. Design/setting/participants /intervention/measurements: this analysis was performed on data from a proof-of-concept study, consisting of a 12-week, double-blind, randomized, controlled, multicenter trial, followed by a similarly designed 12-week extension study. Patients with mild ad (mini-mental state examination [mmse] score of 20-26) were randomized to receive active or control product as a 125 ml daily drink. One of the co-primary outcome measures was the 13-item adas-cog. in this analysis, the study population was divided into two subgroups: patients with 'low' baseline adas-cog scores (<25.0) and patients with 'high' baseline adas-cog scores (≥25.0). Repeated measures models (Rmm) were used to determine the relationship between adas-cog score and intervention. Results: a significant treatment effect (F[1,319]=4.0, p=0.046) was shown in patients with 'high' baseline adas-cog, but not in patients with 'low' baseline adas-cog (F[1,250]=1.25, p=0.265). Overall, intake adherence was significantly correlated with adas-cog improvement in the active product group (correlation coefficient=-0.260; p=0.019), but not the control group. Conclusion: these data indicate that baseline adas-cog significantly influenced the effect of souvenaid intervention on adas-cog outcome. a higher intake of active study product was also associated with greater cognitive benefit. these findings highlight the potential benefits of souvenaid in ad patients and warrant confirmation in larger, controlled studies.

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“…Young adult rats generate ~9000 new cells in the SGZ daily; approximately half of them survive (Cameron and McKay, 2001). The surviving cells develop synaptic connections with the entorhinal cortex and the CA3 subfield, thereby integrating into the existing neuronal circuits (van Praag et al, 2002;Toni et al, 2007).…”

Section: Neurogenesis In the Adult Mammalian Brainmentioning

confidence: 99%

Neural stem cells: mechanisms and modeling

Yao

Gage

2012

Protein Cell

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In the adult brain, neural stem cells have been found in two major niches: the hippocampus and the olfactory bulb. Neurons derived from these stem cells contribute to learning, memory, and the autonomous repair of the brain under pathological conditions. Hence, the physiology of adult neural stem cells has become a significant component of research on synaptic plasticity and neuronal disorders. In addition, the recently developed induced pluripotent stem cell technique provides a powerful tool for researchers engaged in the pathological and pharmacological study of neuronal disorders. In this review, we briefly summarize the research progress in neural stem cells in the adult brain and in the neuropathological application of the induced pluripotent stem cell technique.

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Synapse formation on neurons born in the adult hippocampus

Cited by 509 publications

References 50 publications

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Genetic Regulation of Behavioral and Neuronal Responses to Fluoxetine

Efficacy of a medical food on cognition in Alzheimer's Disease: Results from secondary analyses of a randomized, controlled trial

Neural stem cells: mechanisms and modeling

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