Temporal dynamics of hippocampal neurogenesis in chronic neurodegeneration

Gómez-Nicola, Diego; Suzzi, Stefano; Vargas‐Caballero, Mariana; Fransen, Nina L.; Al-Malki, Hussain; Cebrián-Silla, Arantxa; García‐Verdugo, José Manuel; Riecken, Kristoffer; Fehse, Boris; Perry, V. Hugh

doi:10.1093/brain/awu155

Cited by 77 publications

(85 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interestingly, there was increased neurogenesis in the subgranular zone of the dentate gyrus up to age 6 months, and then a decline to the low level of neurogenesis in physiologically aging mice. These findings confirm the recent report on increased hippocampal neurogenesis in the infective form of prion disease (Gomez-Nicola et al, 2014). In the wider perspective of neurodegenerative diseases, animal models of familial Alzheimer's disease more often exhibit decreased hippocampal neurogenesis (Haughey et al, 2002; Rodríguez et al, 2008; Demars et al, 2010), although normal or even increased proliferative response to neurogenic stimuli has been observed (Mirochnic et al, 2009; Perry et al, 2012).…”

Section: Discussionsupporting

confidence: 93%

Chronic Progressive Neurodegeneration in a Transgenic Mouse Model of Prion Disease

et al. 2016

View full text Add to dashboard Cite

Neurodegenerative diseases present pathologically with progressive structural destruction of neurons and accumulation of mis-folded proteins specific for each condition leading to brain atrophy and functional disability. Many animal models exert deposition of pathogenic proteins without an accompanying neurodegeneration pattern. The lack of a comprehensive model hinders efforts to develop treatment. We performed longitudinal quantification of cellular, neuronal and synaptic density, as well as of neurogenesis in brains of mice mimicking for genetic Creutzfeldt-Jacob disease as compared to age-matched wild-type mice. Mice exhibited a neurodegenerative process of progressive reduction in cortical neurons and synapses starting at age of 4–6 months, in accord with neurologic disability. This was accompanied by significant decrease in subventricular/subependymal zone neurogenesis. Although increased hippocampal neurogenesis was detected in mice, a neurodegenerative process of CA1 and CA3 regions associated with impaired hippocampal-dependent memory function was observed. In conclusion, mice exhibit pathological neurodegeneration concomitant with neurological disease progression, indicating these mice can serve as a model for neurodegenerative diseases.

show abstract

Section: Discussionsupporting

confidence: 93%

Chronic Progressive Neurodegeneration in a Transgenic Mouse Model of Prion Disease

et al. 2016

View full text Add to dashboard Cite

show abstract

“…• self-repair informahealthcare.comresponse seems to be consistent with data obtained in postmortem samples of patients with Alzheimer's disease [8,11]. Therefore, it appears logical to suggest that the use of proneurogenic therapies or approaches aimed at re-activating the proliferation of neural stem cells would provide a long-lasting repairing response in chronic neurodegenerative diseases.…”

Section: Abstract: Cell Differentiation • Cell Migration • Neural Stesupporting

confidence: 66%

“…We recently described an increased neurogenic response in the SGZ of animals with prion disease, a paradigm of chronic progressive neurodegeneration. We observed that the early and sustained death of granule neurons is balanced by an increased neurogenic response, preserving the integrity of the dentate gyrus [8]. Similarly, evidence supports that environmental enrichment and/or enhanced physical activity boosts hippocampal neurogenesis and prevents the cognitive decline observed in transgenic models of Alzheimer's disease [9,10].…”

supporting

confidence: 70%

How can we exploit the brain’s ability to repair itself?

Miller

Gómez-Nicola

2014

Expert Review of Neurotherapeutics

Self Cite

View full text Add to dashboard Cite

“…Adult hippocampal neurogenesis has received great attention in past decades for its important role in the maintenance of normal learning and memory function, as well as its role in pathophysiological processes of disease, such as Alzheimer's disease, major depressive disorder, memory deficits, and epilepsy [37][38][39]. Recent data indicate that acute seizures or precipitating insults can induce neurogenesis, whereas the capacity of neuronal recruitment and proliferation substantially decreases in chronic phases of epilepsy [40].…”

Section: Wnt/b-catenin Signaling Pathway Involved In Neurogenesis Of mentioning

confidence: 99%

The Role of Wnt/β-Catenin Signaling Pathway in Disrupted Hippocampal Neurogenesis of Temporal Lobe Epilepsy: A Potential Therapeutic Target?

Huang

Zhou

et al. 2015

Neurochem Res

View full text Add to dashboard Cite

Temporal lobe epilepsy is one of the most common clinical neurological disorders. One of the major pathological findings in temporal lobe epilepsy is hippocampal sclerosis, characterized by massive neuronal loss and severe gliosis. The epileptogenesis process of temporal lobe epilepsy usually starts with initial precipitating insults, followed by neurodegeneration, abnormal hippocampus circuitry reorganization, and the formation of hypersynchronicity. Experimental and clinical evidence strongly suggests that dysfunctional neurogenesis is involved in the epileptogenesis. Recent data demonstrate that neurogenesis is induced by acute seizures or precipitating insults, whereas the capacity of neuronal recruitment and proliferation substantially decreases in the chronic phase of epilepsy. Participation of the Wnt/β-catenin signaling pathway in neurogenesis reveals its importance in epileptogenesis; its dysfunction contributes to the structural and functional abnormality of temporal lobe epilepsy, while rescuing this pathway exerts neuroprotective effects. Here, we summarize data supporting the involvement of Wnt/β-catenin signaling in the epileptogenesis of temporal lobe epilepsy. We also propose that the Wnt/β-catenin signaling pathway may serve as a promising therapeutic target for temporal lobe epilepsy treatment.

show abstract

Temporal dynamics of hippocampal neurogenesis in chronic neurodegeneration

Cited by 77 publications

References 65 publications

Chronic Progressive Neurodegeneration in a Transgenic Mouse Model of Prion Disease

Chronic Progressive Neurodegeneration in a Transgenic Mouse Model of Prion Disease

How can we exploit the brain’s ability to repair itself?

The Role of Wnt/β-Catenin Signaling Pathway in Disrupted Hippocampal Neurogenesis of Temporal Lobe Epilepsy: A Potential Therapeutic Target?

Contact Info

Product

Resources

About