Aβ increases neural stem cell activity in senescence-accelerated SAMP8 mice

Díaz-Moreno, María; Hortigüela, Rafael; Gonçalves, Ania; Manich, Gemma; García-Bermúdez, Edurne; Moreno-Estellés, Mireia; Eguiluz, César; Vilaplana, Jordi; Pelegrí, Carme; Vilar, Marçal; Mira, Helena

doi:10.1016/j.neurobiolaging.2013.05.011

Cited by 36 publications

(43 citation statements)

References 96 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although an overall trend of impaired neurocyte proliferation in these areas in AD has been documented [32,33,34,35], Kamphuis et al . [36] and Díaz-Moreno et al [37] observed enhanced proliferation in APP/PS1 and SAMP8 mice, respectively. In our study, dramatic increases in the numbers of BrdU-immunoreactive cells in the SVZ and SGZ were observed in AD mice compared with controls.…”

Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Zhang

Fang

et al. 2014

IJMS

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a common neurodegenerative disease in elderly individuals, and effective therapies are unavailable. This study was designed to investigate the neuroprotective effects of sulforaphane (an activator of NF-E2-related factor 2) on mice with AD-like lesions induced by combined administration of aluminum and d-galactose. Step-down-type passive avoidance tests showed sulforaphane ameliorated cognitive impairment in AD-like mice. Immunohistochemistry results indicated sulforaphane attenuated cholinergic neuron loss in the medial septal and hippocampal CA1 regions in AD-like mice. However, spectrophotometry revealed no significant difference in acetylcholine level or the activity of choline acetyltransferase or acetylcholinesterase in the cerebral cortex among groups of control and AD-like mice with and without sulforaphane treatment. Sulforaphane significantly increased the numbers of 5-bromo-2'-deoxyuridine-positive neurons in the subventricular and subgranular zones in AD-like mice which were significantly augmented compared with controls. Atomic absorption spectrometry revealed significantly lower aluminum levels in the brains of sulforaphane-treated AD-like mice than in those that did not receive sulforaphane treatment. In conclusion, sulforaphane ameliorates neurobehavioral deficits by reducing cholinergic neuron loss in the brains of AD-like mice, and the mechanism may be associated with neurogenesis and aluminum load reduction. These findings suggest that phytochemical sulforaphane has potential application in AD therapeutics.

show abstract

Section: Resultsmentioning

confidence: 99%

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Zhang

Fang

et al. 2014

IJMS

View full text Add to dashboard Cite

show abstract

“…In contrast to physiological aging, Aβ is able to increase NSC activity at the earliest steps of AD pathogenesis followed by later decline (Heo et al, 2007; Diaz-Moreno et al, 2013). Furthermore, EE was reported to increase Aβ accumulation in the transgenic AD model mice due to extensive synaptic activity (Jankowsky et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

“…NS-forming capacity is a parameter which is widely used for the assessment of neurogenic potential of neural stem/progenitor cells as well as the action of regulatory molecules, neurotoxic substances, or drug candidates (Pacey et al, 2006). Positive effects of EE on neurogenesis in vivo have been shown (Monteiro et al, 2014; Clemenson et al, 2015), however, there are very limited data on NS development in vitro in AD or aging (Heo et al, 2007; Diaz-Moreno et al, 2013). …”

Section: Introductionmentioning

confidence: 99%

Differential Roles of Environmental Enrichment in Alzheimer’s Type of Neurodegeneration and Physiological Aging

Salmin

Komleva

Кувачева

et al. 2017

Front. Aging Neurosci.

View full text Add to dashboard Cite

Impairment of hippocampal adult neurogenesis in aging or degenerating brain is a well-known phenomenon caused by the shortage of brain stem cell pool, alterations in the local microenvironment within the neurogenic niches, or deregulation of stem cell development. Environmental enrichment (EE) has been proposed as a potent tool to restore brain functions, to prevent aging-associated neurodegeneration, and to cure neuronal deficits seen in neurodevelopmental and neurodegenerative disorders. Here, we report our data on the effects of environmental enrichment on hippocampal neurogenesis in vivo and neurosphere-forming capacity of hippocampal stem/progenitor cells in vitro. Two models – Alzheimer’s type of neurodegeneration and physiological brain aging – were chosen for the comparative analysis of EE effects. We found that environmental enrichment greatly affects the expression of markers specific for stem cells, progenitor cells and differentiated neurons (Pax6, Ngn2, NeuroD1, NeuN) in the hippocampus of young adult rats or rats with Alzheimer’s disease (AD) model but less efficiently in aged animals. Application of time-lag mathematical model for the analysis of impedance traces obtained in real-time monitoring of cell proliferation in vitro revealed that EE could restore neurosphere-forming capacity of hippocampal stem/progenitor cells more efficiently in young adult animals (fourfold greater in the control group comparing to the AD model group) but not in the aged rats (no positive effect of environmental enrichment at all). In accordance with the results obtained in vivo, EE was almost ineffective in the recovery of hippocampal neurogenic reserve in vitro in aged, but not in amyloid-treated or young adult, rats. Therefore, EE-based neuroprotective strategies effective in Aβ-affected brain could not be directly extrapolated to aged brain.

show abstract

“…Transplantation of human adipose tissuederived MSCs improved both locomotor activity and cognitive function in the aged animals, in parallel with the recovery of acetylcholine levels in brain tissues, which was accomplished by enhancing the concentrations of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) [41] , and vascular endothelial growth factor (VEGF) [42] . Aβ increases NSPC activity [43] , which may be a natural reaction against toxicity induced by AD. After conditional neuronal ablation in the hippocampus, NSPCs survived, migrated, differentiated, and, most significantly, improved memory after being transplanted into the brain [44] .…”

Section: Exogenous Stem Cellsmentioning

confidence: 99%

Cell-based therapy in Alzheimer's disease: Current knowledge and perspective

Qiao

Huang²,

Chen

2016

Transl. Neurosci. Clin.

View full text Add to dashboard Cite

KEYWORDSAlzheimer's disease; cell therapy; stem cells; neurogenesis Alzheimer's disease (AD) is the most prevalent type of dementia, and its neuropathology is characterized by the deposition of insoluble β-amyloid (Aβ) peptides, intracellular neurofibrillary tangles, amyloid angiopathy, age-related brain atrophy, synaptic pathology, white matter rarefaction, granulovacuolar degeneration, neuron loss, and neuroinflammation. Although much is known about the neurobiology of AD, very few conventional therapies are available to arrest or slow the disease. There is an urgent need for novel therapeutic approaches for AD. AD subjects have significantly fewer viable precursor cells in the hippocampus compared with age-matched healthy control subjects. However, the viable precursor cells that remain in AD and age-matched healthy control brain specimens can be induced to differentiate. To facilitate or mimic the natural compensatory effect in AD, cell therapy, including endogenous and exogenous stem cells, has been considered in AD. In this review, we focus on the history and development of cell therapy in AD, and consider the role of cell therapy as a potential treatment for AD.Citation Qiao LY, Huang HY, Chen L. Cell-based therapy in Alzheimer's disease: Current knowledge and perspective. Transl. Neurosci. Clin. 2016, 2(1): 50-58.

show abstract

Aβ increases neural stem cell activity in senescence-accelerated SAMP8 mice

Cited by 36 publications

References 96 publications

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Neuroprotective Effects of Sulforaphane on Cholinergic Neurons in Mice with Alzheimer’s Disease-Like Lesions

Differential Roles of Environmental Enrichment in Alzheimer’s Type of Neurodegeneration and Physiological Aging

Cell-based therapy in Alzheimer's disease: Current knowledge and perspective

Contact Info

Product

Resources

About