Chronic noise exposure causes persistence of tau hyperphosphorylation and formation of NFT tau in the rat hippocampus and prefrontal cortex

Cui, Bo; Zhu, Lixing; She, Xiaojun; Wu, Mingquan; Ma, Qiang; Wang, Tianhui; Zhang, Na; Xu, Chuan-Xiang; Chen, Xuewei; An, Gaihong; Liu, Hongtao

doi:10.1016/j.expneurol.2012.08.028

Cited by 62 publications

(59 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Using Western blot, we used three antibodies targeting several key tau phosphoepitopes. The phosphorylated tau antibodies detected pre-neurofibrillary tangle phospho-tau protein (pThr 231 ), intraneuronal neurofibrillary tangle phospho-tau protein (pSer 214 ), and extracellular neurofibrillary tangle phospho-tau protein (pSer 404 ) according to earlier studies (Augustinack et al, 2002, Cui et al, 2012). Our results showed no significant group differences in total tau levels (F(3,36) = 5.05, p=0.11) but a significant increased in hippocampal tau phosphorylation at the pre-tangle (F(3,36) = 9.75, p<0.05), intraneuronal tangle (F(3,36) = 9.59, p<0.05), and extracellular tangle sites (F(3,36) = 10.02, p<0.05) were seen in the aged rats compared to the young animals (Fig.…”

Section: Resultsmentioning

confidence: 56%

Retraction notice to “DECREASE IN AGE-RELATED TAU HYPERPHOSPHORYLATION AND COGNITIVE IMPROVEMENT FOLLOWING VITAMIN D SUPPLEMENTATION ARE ASSOCIATED WITH MODULATION OF BRAIN ENERGY METABOLISM AND REDOX STATE” Neuroscience 262 (2014) 143–155

Briones

Darwish

2014

Neuroscience

View full text Add to dashboard Cite

In the present study we examined whether vitamin D supplementation can reduce age-related tau hyperphosphorylation and cognitive impairment by enhancing brain energy homeostasis and protein phosphatase-2A (PP2A) activity, and modulating the redox state. Male F344 rats age 20 months (aged) and 6 months (young) were randomly assigned to either vitamin D supplementation or no supplementation (control). Rats were housed in pairs and the supplementation group (n=10 young and n=10 aged) received subcutaneous injections of vitamin D (1, α25-dihydroxyvitamin D3) for 21 days. Control animals (N=10 young and n=10 aged) received equal volume of normal saline and behavioral testing in water maze started on day 14 after initiation of vitamin D supplementation. Tau phosphorylation, markers of brain energy metabolism (ADP/ATP ratio and adenosine monophosphate-activated protein kinase) and redox state (levels of reactive oxygen species, activity of superoxide dismutase, and glutathione levels) as well as PP2A activity were measured in hippocampal tissues. Our results extended previous findings that: 1) tau phosphorylation significantly increased during aging; 2) markers of brain energy metabolism and redox state are significantly decreased in aging; and 3) aged rats demonstrated significant learning and memory impairment. More importantly, we found that age-related changes in brain energy metabolism, redox state, and cognitive function were attenuated by vitamin D supplementation. No significant differences were seen in tau hyperphosphorylation, markers of energy metabolism and redox state in the young animal groups. Our data suggests that vitamin D ameliorated the age-related tau hyperphosphorylation and cognitive decline by enhancing brain energy metabolism, redox state, and PP2A activity making it a potentially useful therapeutic option to alleviate the effects of aging.

show abstract

Section: Resultsmentioning

confidence: 56%

Retraction notice to “DECREASE IN AGE-RELATED TAU HYPERPHOSPHORYLATION AND COGNITIVE IMPROVEMENT FOLLOWING VITAMIN D SUPPLEMENTATION ARE ASSOCIATED WITH MODULATION OF BRAIN ENERGY METABOLISM AND REDOX STATE” Neuroscience 262 (2014) 143–155

Briones

Darwish

2014

Neuroscience

View full text Add to dashboard Cite

show abstract

“…For instance, an impairment in a sensory pathway may reduce the quality of input received by the cognitive domain thus compromising cognitive function, e.g. hippocampal function (336–339); an impairment in the cognitive domain could reduce its modulatory effect on the sensory pathway as well as diminish its control of motor output generation, leading to both altered sensory responses and motor output patterns; while an impairment in the motor pathway may impede the proper transmission of the commands from the cognitive domain, thus resulting in uncoordinated motor patterns and inefficient capture of environmental signals. Given this interdependence of sensory, motor, and cognitive systems, changes in sensory or motor function may either cause or reflect subtle deficits in the cognitive processes prior to the progression to more severe cognitive impairment conditions.…”

Section: Discussionmentioning

confidence: 99%

“…One view is that the dysfunction occurs in parallel with the development of the disease in the association cortices and hippocampus. By contrast, the dysfunction in the sensory systems may represent a primary disturbance to the expected input into the association cortices and the hippocampus, which triggers pathological plasticity processes (339). For instance, altered neuronal activity was shown to reduce the transport and release of the neurotrophic factor BDNF by Christine Gall and Gary Lynch (350).…”

Section: Discussionmentioning

confidence: 99%

At the interface of sensory and motor dysfunctions and Alzheimer's disease

Albers

Gilmore

Kaye

et al. 2014

Alzheimer's & Dementia

463

379

View full text Add to dashboard Cite

Recent evidence indicates that sensory and motor changes may precede the cognitive symptoms of Alzheimer’s disease (AD) by several years and may signify increased risk of developing AD. Traditionally, sensory and motor dysfunctions in aging and AD have been studied separately. To ascertain the evidence supporting the relationship between age-related changes in sensory and motor systems and the development of AD and to facilitate communication between several disciplines, the National Institute on Aging held an exploratory workshop titled “Sensory and Motor Dysfunctions in Aging and Alzheimer’s Disease”. The scientific sessions of the workshop focused on age-related and neuropathological changes in the olfactory, visual, auditory, and motor systems, followed by extensive discussion and hypothesis generation related to the possible links among sensory, cognitive, and motor domains in aging and AD. Based on the data presented and discussed at this workshop, it is clear that sensory and motor regions of the CNS are affected by Alzheimer pathology and that interventions targeting amelioration of sensory-motor deficits in AD may enhance patient function as AD progresses.

show abstract

“…This phosphorylation took place in at least two of the phospho-TAU epitopes (pThr231 and pSer262) upregulated by stress that were strongly implicated in the neuropathology of AD (Kimura et al, 2007;Mazanetz and Fischer, 2007;Sotiropoulos et al, 2008). Cui et al (2012) showed that chronic noise exposure causes persistence of TAU hyperphosphorylation and formation of neurofibrillary tangles in the rat HC and PFC. Moreover, Filipcik et al (2012) found TAU protein phosphorylation in diverse brain areas of normal and CRH deficient mice that was up-regulated by stress.…”

Section: Tau Hyperphosphorylationmentioning

confidence: 97%

Chronic stress as a risk factor for Alzheimer’s disease

Machado¹,

Herrera²,

Pablos³

et al. 2014

Reviews in the Neurosciences

150

View full text Add to dashboard Cite

AbstractThis review aims to point out that chronic stress is able to accelerate the appearance of Alzheimer’s disease (AD), proposing the former as a risk factor for the latter. Firstly, in the introduction we describe some human epidemiological studies pointing out the possibility that chronic stress could increase the incidence, or the rate of appearance of AD. Afterwards, we try to justify these epidemiological results with some experimental data. We have reviewed the experiments studying the effect of various stressors on different features in AD animal models. Moreover, we also point out the data obtained on the effect of chronic stress on some processes that are known to be involved in AD, such as inflammation and glucose metabolism. Later, we relate some of the processes known to be involved in aging and AD, such as accumulation of β-amyloid, TAU hyperphosphorylation, oxidative stress and impairement of mitochondrial function, emphasizing how they are affected by chronic stress/glucocorticoids and comparing with the description made for these processes in AD. All these data support the idea that chronic stress could be considered a risk factor for AD.

show abstract

Chronic noise exposure causes persistence of tau hyperphosphorylation and formation of NFT tau in the rat hippocampus and prefrontal cortex

Cited by 62 publications

References 42 publications

Retraction notice to “DECREASE IN AGE-RELATED TAU HYPERPHOSPHORYLATION AND COGNITIVE IMPROVEMENT FOLLOWING VITAMIN D SUPPLEMENTATION ARE ASSOCIATED WITH MODULATION OF BRAIN ENERGY METABOLISM AND REDOX STATE” Neuroscience 262 (2014) 143–155

Retraction notice to “DECREASE IN AGE-RELATED TAU HYPERPHOSPHORYLATION AND COGNITIVE IMPROVEMENT FOLLOWING VITAMIN D SUPPLEMENTATION ARE ASSOCIATED WITH MODULATION OF BRAIN ENERGY METABOLISM AND REDOX STATE” Neuroscience 262 (2014) 143–155

At the interface of sensory and motor dysfunctions and Alzheimer's disease

Chronic stress as a risk factor for Alzheimer’s disease

Contact Info

Product

Resources

About