Effects of streptozotocin-induced diabetes on tau phosphorylation in the rat brain

Qu, Zhongsen; Zhang, Jiao; Sun, Xiaojiang; Zhao, Yuwu; Ren, Jun; Xu, Guogang

doi:10.1016/j.brainres.2011.01.084

Cited by 79 publications

(58 citation statements)

References 30 publications

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“…A result that indicates a decrease in the level and/or activity of the enzyme. The result of the current study is in harmony with previous reports [38,46].…”

Section: Discussionsupporting

confidence: 95%

“…STZ-induced diabetes resulted in a noticeable increase in the gene expression of the enzyme glycogen synthase kinase-3b (GSK-3b) in the hippocampal tissues of diabetic rats as compared with normal control rats as proved by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) test. This result reflects increased activity of that enzyme which was parallel to previous reports [10,37,38].…”

Section: Discussionsupporting

confidence: 88%

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Effect of Imipramine, Paroxetine, and Lithium Carbonate on Neurobehavioral Changes of Streptozotocin in Rats: Impact on Glycogen Synthase Kinase-3 and Blood Glucose Level

Nadeem¹,

Ahmed

El-Denshary

2015

Neurochem Res

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Recent studies have demonstrated a scrutinized association of diabetes mellitus with depressive symptoms and major depression. Glycogen synthase kinase-3 (GSK-3) is a protein kinase enzyme constitutively active in non-stimulated cells and in multiple signalings. Independent lines of research provide a converging evidence for an involvement of GSK-3 in the regulation of behavior and hyperglycemia. The present study revealed that streptozotocin (STZ)-induced diabetic rats were found to show lengthened duration of immobility in the forced-swimming test (FST) and reduced locomotor and exploratory activities in the open-field test (OFT). Imipramine (15 mg/kg), Paroxetine (10 mg/kg) and lithium carbonate (36.94 mg/kg) for 14 days reduced immobility behavior in FST. Paroxetine and lithium carbonate increased the locomotor and exploratory activities, while imipramine decreased the locomotor activity in the OFT. Imipramine and lithium carbonate reduced the blood glucose level while paroxetine didn't alter it. STZ-induced diabetes increased GSK-3 gene expression which was determined using the reverse transcription-quantitative polymerase chain reaction test, while the three drugs decreased its expression. It can be concluded that lithium carbonate and imipramine can control both hyperglycemia and the associated symptoms of depression at the same time by inhibiting GSK-3 activity. On the other hand, paroxetine may only manage the depressive-like symptoms associated with diabetes through modulating the enzyme GSK-3, without changing blood glucose levels.

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“…A result that indicates a decrease in the level and/or activity of the enzyme. The result of the current study is in harmony with previous reports [38,46].…”

Section: Discussionsupporting

confidence: 95%

Section: Discussionsupporting

confidence: 88%

Effect of Imipramine, Paroxetine, and Lithium Carbonate on Neurobehavioral Changes of Streptozotocin in Rats: Impact on Glycogen Synthase Kinase-3 and Blood Glucose Level

Nadeem¹,

Ahmed

El-Denshary

2015

Neurochem Res

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“…Jolivalt демонстрируют нарушение сигнального пути инсулина и активности фосфорилирования тау-белка после 9 недель стрепто-зотоцин-индуцированного диабета в мозге мышей [35]. Таким образом, дефекты сигнальных путей инсулина имеют основополагающее значение для развития когни-тивных нарушений, которые могут возникать либо от де-фицита инсулина (СД1), либо вследствие резистентности к инсулину (СД2), вызывая аномальную активацию GSK-3 [36][37][38][39][40]. Данные влияния различных тау-фосфа-таз на моделях с СД на развитие когнитивных наруше-ний мало изучены по сравнению с GSK-3 .…”

Section: сахарный диабет и таупатияunclassified

“…Интересно отметить, что генетическое удаление тау-белка предотвращает на-рушение памяти. Кроме того, абляции белка смягчают течение диабет-индуцированных когнитивных наруше-ний [52,53]. Взятые вместе, эти данные свидетельствуют о том, что при СД происходит гиперфосфорилирование тау-протеина вследствие нарушения сигналов инсулина в головном мозге, которое вносит свой вклад в когнитив-ные нарушения.…”

Section: сахарный диабет Diabetes Mellitus 183unclassified

Tauopathy and cognitive impairment in experimental diabetes mellitus

et al. 2017

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Обучение и психосоциальные аспекты Education and psychosocial aspectТаупатии и когнитивные нарушения ау-протеин, ассоциированный с микротрубоч-ками центральной нервной системы (ЦНС), представляет собой белок цитоскелета, регули-рующий развитие нейронов и способствующий сборке и стабильности микротрубочек, которые являются важ-ными для транспорта везикул в ЦНС. В человеческом мозге семейство тау-белков представлено шестью изо-формами в диапазоне от 352 до 441 аминокислот, получен-ных из одного гена путем альтернативного сплайсинга [1]. Амино-концевой остаток тау-протеина (или «область проекции» микротрубочек) взаимодействует с плаз-матической мембраной. Карбоксиконцевая область характеризуется наличием 3 или 4 повторов, которые обе-спечивают свойства тау-белков для стабилизации микро-трубочек, способствуют их полимеризации. Эти функции негативно регулируются с помощью фосфорилирования в нескольких местах (и вокруг) связывающего домена ми-кротрубочек. Этот процесс может проходить с участием нескольких киназ [2,3]. Почти 20% от тау-белка фосфо-рилируется в физиологических условиях [4]. Внутрикле-точные агрегаты избыточно гиперфосфорилированного тау-белка характеризуют группу нейродегенеративных заболеваний под названием «таупатии» [5,6,7]. Все та-упатии делятся на спорадические нейродегенеративные заболевания (прогрессирующий надъядерный паралич, мультисистемная атрофия, деменция с тельцами Леви, болезнь Альцгеймера (БА) и др.) и ирритативные (болезнь Гентингтона, Вильсона-Коновалова, Фара и др.) [8].Патогенез таупатий включает накопление тау-белка в головном мозге и прогрессирующее нарушение ра-

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“…Furthermore, acute insulin administration improves memory in both humans and rodents (Craft et al, 2012; Park et al, 2000; Watson et al, 2006), and disruption of CNS insulin signaling leads to cognitive deficits in rodents (Lannert and Hoyer, 1998; Steen et al, 2005). Subsequent studies in animal models for insulin resistance, AD, or both, have established that insulin resistance exacerbates Aβ and tau phenotypes including enhanced Aβ 42/40 ratio, total tau, and hyperphosphorylated tau (Ho et al, 2004; Lester-Coll et al, 2006; Li et al, 2007; Masciopinto et al, 2012; Plaschke et al, 2010; Qu et al, 2011; Searcy et al, 2012; Takeda et al, 2010) and AD amyloidosis models exhibit insulin resistance (Rodriguez-Rivera et al, 2011). …”

Section: Alzheimer's Diseasementioning

confidence: 99%

Insulin resistance in Alzheimer's disease

Dineley

Jahrling

Denner

2014

Neurobiology of Disease

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Insulin is a key hormone regulating metabolism. Insulin binding to cell surface insulin receptors engages many signaling intermediates operating in parallel and in series to control glucose, energy, and lipids while also regulating mitogenesis and development. Perturbations in the function of any of these intermediates, which occur in a variety of diseases, cause reduced sensitivity to insulin and insulin resistance with consequent metabolic dysfunction. Chronic inflammation ensues which exacerbates compromised metabolic homeostasis. Since insulin has a key role in learning and memory as well as directly regulating ERK, a kinase required for the type of learning and memory compromised in early Alzheimer's disease (AD), insulin resistance has been identified as a major risk factor for the onset of AD. Animal models of AD or insulin resistance or both demonstrate that AD pathology and impaired insulin signaling form a reciprocal relationship. Of note are human and animal model studies geared toward improving insulin resistance that have led to the identification of the nuclear receptor and transcription factor, peroxisome proliferator-activated receptor gamma (PPARγ) as an intervention tool for early AD. Strategic targeting of alternate nodes within the insulin signaling network has revealed disease-stage therapeutic windows in animal models that coalesce with previous and ongoing clinical trial approaches. Thus, exploiting the connection between insulin resistance and AD provides powerful opportunities to delineate therapeutic interventions that slow or block the pathogenesis of AD.

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Effects of streptozotocin-induced diabetes on tau phosphorylation in the rat brain

Cited by 79 publications

References 30 publications

Effect of Imipramine, Paroxetine, and Lithium Carbonate on Neurobehavioral Changes of Streptozotocin in Rats: Impact on Glycogen Synthase Kinase-3 and Blood Glucose Level

Effect of Imipramine, Paroxetine, and Lithium Carbonate on Neurobehavioral Changes of Streptozotocin in Rats: Impact on Glycogen Synthase Kinase-3 and Blood Glucose Level

Tauopathy and cognitive impairment in experimental diabetes mellitus

Insulin resistance in Alzheimer's disease

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