Thyroid hormone prevents cognitive deficit in a mouse model of Alzheimer's disease

Fu, Ai; Zhou, Cheng; Chen, Xiang

doi:10.1016/j.neuropharm.2009.12.020

Cited by 58 publications

(41 citation statements)

References 51 publications

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“…In adults, the mechanisms underlying these cognitive problems are less well understood than during perinatal development. However, it is established that reduced neurogenesis, especially in the rodent hippocampus, due to either aging or stress, is associated with neurocognitive deficits such as anxiety, depression (6), and with neurodegenerative disease such as Alzheimer’s (7, 8). In mammals, including humans, the subgranular zone (SGZ) of the hippocampal dentate gyrus and the subventricular zone (SVZ) represent the two main neurogenic niches.…”

Section: Thyroid Hormones and Adult Brain Functionmentioning

confidence: 99%

“…Marked effects are seen on learning and memory, processes that implicate neurogenesis in the dentate gyrus of the hippocampus (62, 63), a structure that diminishes with age and in many neurodegenerative pathologies (62, 64). TH treatment can improve cognitive performances in hypothyroid mice (8) and in humans (65), leading to speculation that cognitive deficiency can be causally linked to reduced TH signaling in aging. Despite declining neurogenesis with age, Yeung et al recently demonstrated that 13-month-old mice still have the capacity to generate new neurons after a selective neuronal loss in the hippocampus, but without cognitive recovery (66).…”

Section: Th Control Of Adult Neurogenesis In the Aging Brainmentioning

confidence: 99%

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Thyroid Hormone Signaling and Adult Neurogenesis in Mammals

et al. 2014

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The vital roles of thyroid hormone in multiple aspects of perinatal brain development have been known for over a century. In the last decades, the molecular mechanisms underlying effects of thyroid hormone on proliferation, differentiation, migration, synaptogenesis, and myelination in the developing nervous system have been gradually dissected. However, recent data reveal that thyroid signaling influences neuronal development throughout life, from early embryogenesis to the neurogenesis in the adult brain. This review deals with the latter phase and analyses current knowledge on the role of T3, the active form of thyroid hormone, and its receptors in regulating neural stem cell function in the hippocampus and the subventricular zone, the two principal sites harboring neurogenesis in the adult mammalian brain. In particular, we discuss the critical roles of T3 and TRα1 in commitment to a neuronal phenotype, a process that entails the repression of a number of genes notably that encoding the pluripotency factor, Sox2. Furthermore, the question of the relevance of thyroid hormone control of adult neurogenesis is considered in the context of brain aging, cognitive decline, and neurodegenerative disease.

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Section: Thyroid Hormones and Adult Brain Functionmentioning

confidence: 99%

Section: Th Control Of Adult Neurogenesis In the Aging Brainmentioning

confidence: 99%

Thyroid Hormone Signaling and Adult Neurogenesis in Mammals

et al. 2014

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“…We have previously shown that the synthetic form of thyroxine, L-T4, prevents cognitive deficits and improves neurological function in an AD mouse model[13]. This study aimed to assess whether L-T4 improves cognitive impairment in memory-deficient aged mice by increasing superoxide dismutase activity, cholinergic function, and cytoskeleton rearrangement.…”

Section: Introductionmentioning

confidence: 99%

The synthetic thyroid hormone, levothyroxine, protects cholinergic neurons in the hippocampus of naturally aged mice

Zhou

2014

Neural Regen Res

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The thyroid hormones, triiodothyronine and thyroxine, play important roles in cognitive function during the mammalian lifespan. However, thyroid hormones have not yet been used as a therapeutic agent for normal age-related cognitive deficits. In this study, CD-1 mice (aged 24 months) were intraperitoneally injected with levothyroxine (L-T4; 1.6 μg/kg per day) for 3 consecutive months. Our findings revealed a significant improvement in hippocampal cytoskeletal rearrangement of actin and an increase in serum hormone levels of L-T4-treated aged mice. Furthermore, the survival rate of these mice was dramatically increased from 60% to 93.3%. The Morris water maze task indicated that L-T4 restored impaired spatial memory in aged mice. Furthermore, level of choline acetyltransferase, acetylcholine, and superoxide dismutase were increased in these mice, thus suggesting that a possible mechanism by which L-T4 reversed cognitive impairment was caused by increased activity of these markers. Overall, supplement of low-dosage L-T4 may be a potential therapeutic strategy for normal age-related cognitive deficits.

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“…The authors suggested that the mechanisms of LT4 treating AD might be associated with regulating cholinergic function, protecting the brains of AD model mice against damage and rescuing hippocampal neurons from apoptosis. The results of this study seem indicate that the use of thyroid hormone may have some therapeutic potential in AD (Fu et al, 2010). Accordingly, in a post mortem study it was evaluated the brain thyroid hormone levels in AD measured with radioimmunoassay (RIA) samples of prefrontal cortex of patients with pathologically confirmed AD and controls without any primary neurological disease.…”

Section: Thyroid Function and Cognitive Impairmentmentioning

confidence: 99%