Relationship of Adult Neurogenesis with Tau Phosphorylation and GSK-3β Activity in Subventricular Zone

Hong, Xiaoping; Peng, Caixia; Wei, Wei; Tian, Qing; Liu, Yinghua; Cao, Fuliang; Wang, Qun; Wang, Jian‐Zhi

doi:10.1007/s11064-010-0316-y

Cited by 19 publications

(14 citation statements)

References 45 publications

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“…Generation of new neurons becomes impaired in AD. It is important to point out here that phosphorylation of tau significantly contribute to neurogenesis in hippocampal region of brain [98]. Cytoskeleton of cells including microtubules regulate expression of genes, support intracellular structures and transport, contribute to signal transduction and to generation of some growth factors including connective tissue growth factor.…”

Section: Resultsmentioning

confidence: 99%

Inverse relationship between Alzheimer’s disease and cancer, and other factors contributing to Alzheimer’s disease: a systematic review

Shafi

2016

BMC Neurol

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BackgroundThe AD etiology is yet not properly known. Interactions among environmental factors, multiple susceptibility genes and aging, contribute to AD. This study investigates the factors that play role in causing AD and how changes in cellular pathways contribute to AD.MethodsPUBMED database, MEDLINE database and Google Scholar were searched with no date restrictions for published articles involving cellular pathways with roles in cancers, cell survival, growth, proliferation, development, aging, and also contributing to Alzheimer’s disease. This research explores inverse relationship between AD and cancer, also investigates other factors behind AD using several already published research literature to find the etiology of AD.ResultsCancer and Alzheimer’s disease have inverse relationship in many aspects such as P53, estrogen, neurotrophins and growth factors, growth and proliferation, cAMP, EGFR, Bcl-2, apoptosis pathways, IGF-1, HSV, TDP-43, APOE variants, notch signals and presenilins, NCAM, TNF alpha, PI3K/AKT/MTOR pathway, telomerase, ROS, ACE levels. AD occurs when brain neurons have weakened growth, cell survival responses, maintenance mechanisms, weakened anti-stress responses such as Vimentin, Carbonic anhydrases, HSPs, SAPK. In cancer, these responses are upregulated and maintained. Evolutionarily conserved responses and maintenance mechanisms such as FOXO are impaired in AD.Countermeasures or compensatory mechanisms by AD affected neurons such as Tau, Beta Amyloid, S100, are last attempts for survival which may be protective for certain time, or can speed up AD in Alzheimer’s microenvironment via C-ABL activation, GSK3, neuro-inflammation.ConclusionsAlzheimer’s disease and Cancer have inverse relationship; many factors that are upregulated in any cancer to sustain growth and survival are downregulated in Alzheimer’s disease contributing to neuro-degeneration. When aged neurons or genetically susceptible neurons have weakened growth, cell survival and anti-stress responses, age related gene expression changes, altered regulation of cell death and maintenance mechanisms, they contribute to Alzheimer’s disease. Countermeasures by AD neurons such as Beta Amyloid Plaques, NFTs, S100, are last attempts for survival and this provides neuroprotection for certain time and ultimately may become pathological and speed up AD. This study may contribute in developing new potential diagnostic tests, interventions and treatments.Electronic supplementary materialThe online version of this article (doi:10.1186/s12883-016-0765-2) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Inverse relationship between Alzheimer’s disease and cancer, and other factors contributing to Alzheimer’s disease: a systematic review

Shafi

2016

BMC Neurol

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“…Neurogenesis in the brain is influenced by various environmental stimuli including aging and ischemic injury [5][6][7][8][9][10][11][12]. Neurogenesis decreases in intact brain including the DG [13][14][15], and the subventricular zone of the lateral ventricle during the normal aging process [8,9].…”

Section: Introductionmentioning

confidence: 99%

Comparison of Neurogenesis in the Dentate Gyrus Between the Adult and Aged Gerbil Following Transient Global Cerebral Ischemia

Choi

Yoo

Lee³

et al. 2012

Neurochem Res

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In the present study, we compared differences in cell proliferation, neuroblast differentiation and neuronal maturation in the hippocampal dentate gyrus (DG) between the adult and aged gerbil induced by 5 min of transient global cerebral ischemia using Ki-67 and BrdU (markers for cell proliferation), doublecortin (DCX, a marker for neuroblast differentiation) and neuronal nuclei (NeuN, a marker for mature neuron). The number of Ki-67-immunoreactive (⁺) cells in the DG of both the groups peaked 7 days after ischemia/reperfusion (I/R). However, the number in the aged DG was 40.6 ± 1.8% of that in the adult DG. Thereafter, the number decreased with time. After ischemic damage, DCX immunoreactivity and its protein level in the adult and aged DG peaked at 10 and 15 days post-ischemia, respectively. However, DCX immunoreactivity and its protein levels in the aged DG were much lower than those in the adult. DCX immunoreactivity and its protein level in the aged DG were 11.1 ± 0.6% and 34.4 ± 2.1% of the adult DG, respectively. In addition, the number of Ki-67⁺ cells and DCX immunoreactivity in both groups were similar to those in the sham at 60 days postischemia. At 30 days post-ischemia, the number of BrdU⁺ cells and BrdU⁺/NeuN⁺ cells in the adult-group were much higher (281.2 ± 23.4% and 126.4 ± 7.4%, respectively) than the aged-group (35.6 ± 6.8% and 79.5 ± 6.1%, respectively). These results suggest that the ability of neurogenesis in the ischemic aged DG is much lower than that in the ischemic adult DG.

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“… 45 Levels of Tau phosphorylation also increase in the SVZ with age, and are higher in the SVZ than in other regions of the brain. 75 The SVZ of AD patients also has significantly less proliferating precursor cells than normal, 76 which further exacerbates age-dependent cognitive decline due to a failure of homeostatic regeneration by differentiating neuroblasts in target brain regions. In addition to the reduced SVZ neurogenic potential that accompanies normal aging, a dysregulation of Tau phosphorylation within SVZ precursor neurons may dramatically affect the capacity of the 3R Tau-enriched neural precursor population to successfully migrate and differentiate, and thus further contribute to AD pathology( Fig.…”

Section: Neuroplasticity – a Liability In The Face Of Tau Dysregulatimentioning

confidence: 99%

Temperature and toxic Tau in Alzheimer's disease: new insights

et al. 2015

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Alzheimer's disease (AD), the most common dementia in the elderly, is characterized by cognitive impairment and severe autonomic symptoms such as disturbance in core body temperature (Tc), which may be predictors or early events in AD onset. Inclusions of phosphorylated Tau (p-Tau) are a hallmark of AD and other neurodegenerative disorders called “Tauopathies.” Animal and human studies show that anesthesia augments p-Tau levels through reduction of Tc, with implications for AD. Additionally, hypothermia impairs memory and cognitive function. The molecular networks related to Tc that are associated with AD remain poorly characterized. Under physiological conditions, Tau binds microtubules, promoting their assembly and stability. The dynamically regulated Tau-microtubule interaction plays an important role in structural remodeling of the cytoskeleton, having important functions in neuronal plasticity and memory in the hippocampus. Hypothermia-induced increases in p-Tau levels are significant, with an 80% increase for each degree Celsius below normothermic conditions. Although the effects of temperature on Tau phosphorylation are evident, its effects on p-Tau degradation remain poorly understoodWe review information concerning the mechanisms of Tau regulation of neuron plasticity via its effects on microtubule dynamics, with focus on pathways regulating the abundance of phosphorylated Tau species. We highlight the effects of temperature on molecular mechanisms influencing the development of Tau-related diseases. Specifically, we argue that cold might preferentially affects central nervous system structures that are highly reliant upon plasticity, such as the hippocampus, and that the effect of cold on Tau phosphorylation may constitute a pathology-initiating trigger leading to neurodegeneration.

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Relationship of Adult Neurogenesis with Tau Phosphorylation and GSK-3β Activity in Subventricular Zone

Cited by 19 publications

References 45 publications

Inverse relationship between Alzheimer’s disease and cancer, and other factors contributing to Alzheimer’s disease: a systematic review

Inverse relationship between Alzheimer’s disease and cancer, and other factors contributing to Alzheimer’s disease: a systematic review

Comparison of Neurogenesis in the Dentate Gyrus Between the Adult and Aged Gerbil Following Transient Global Cerebral Ischemia

Temperature and toxic Tau in Alzheimer's disease: new insights

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