Antidepressants for neuro-regeneration: from depression to Alzheimer’s disease

Kim, Hyun-Jung; Kim, Woosuk; Kong, Sun-Young

doi:10.1007/s12272-013-0238-8

Cited by 31 publications

(18 citation statements)

References 129 publications

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“…BDNF could also increase the expression of the vesicle proteins synaptophysin, synaptobrevin, and synaptotagmin and their postsynaptic protein expression [48][49][50]. Enhancement of neurotrophic effects of BDNF by activation of the CREB/pCREB/BDNF signaling pathway was considered as a main molecular mechanism of the therapeutical effect of fluoxetine on AD [51]. Our results also showed that fluoxetine exposure increased the expression of synaptic-related protein levels in the hippocampus of 3 × TgAD mice via activating the CREB/p-CREB/BDNF signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Long-term Ameliorative Effects of the Antidepressant Fluoxetine Exposure on Cognitive Deficits in 3 × TgAD Mice

et al. 2016

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Fluoxetine, a selective serotonin reuptake inhibitor, is neuroprotective; therefore, it has been applied to treat some neurodegenerative disorders. For instance, chronic fluoxetine exposure has short-term effects on Alzheimer's disease (AD). However, the long-term ameliorative effects of fluoxetine exposure on AD have not been reported. In the present study, 6-month-old 3 × TgAD mice were treated with fluoxetine for 15 days, and then the influence of fluoxetine was detected at 20 days after the drug withdrawal. We found that chronic fluoxetine treatment ameliorated cognitive deficits of 3 × TgAD mice and increased the volume of the hippocampal CA1 and dentate gyrus (DG) with increased neuron number and dendritic spine density. Meanwhile, fluoxetine exposure also stimulated the long-term potentiation (LTP) in hippocampal DG. The synaptic-related protein expression increased via activation of the cyclic AMP response element binding (CREB) protein/brain-derived neurotrophic factor (BDNF) signaling pathway induced by fluoxetine exposure. Lastly, we found that fluoxetine treatment decreased beta-amyloid (Aβ) levels. These results further certified that fluoxetine may be a potent effective drug for AD.

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Section: Discussionmentioning

confidence: 99%

Long-term Ameliorative Effects of the Antidepressant Fluoxetine Exposure on Cognitive Deficits in 3 × TgAD Mice

et al. 2016

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“…This evidence indicates that the AD brain shows abnormalities in the serotonergic system and that increasing the level of 5‐HT in the brain might be a potential cure for AD. In recent years, fluoxetine (FLX) has been used for the treatment of AD patients with depression and anxiety, and FLX shows positive effects on cognition as well as improves mental symptoms in patients with AD (Aboukhatwa, Dosanjh, & Luo, ; Kim, Kim, & Kong, ; Mowla, Mosavinasab, Haghshenas, & Borhani Haghighi, ; Rozzini et al, ). In addition, FLX was found to prevent cognitive deterioration in an animal model of AD (Ivkovic, Damjanovic, Jasovic‐Gasic, & Paunovic, ; Jin et al, ).…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine delays the cognitive function decline and synaptic changes in a transgenic mouse model of early Alzheimer's disease

Zhou

Chao

Zhang

et al. 2019

J of Comparative Neurology

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Alzheimer's disease (AD) is a progressive neurodegenerative disorder associated with cognitive decline. Previous studies have reported that the syndrome of AD begins with subtle alterations in hippocampal synapses prior to frank neuronal degeneration. It has recently been reported that fluoxetine (FLX) shows positive effects on AD patients who have depression and anxiety. However, it is unclear whether FLX can affect the pathogenesis of AD mice in the early stage of AD. To address this question, 8‐month‐old male APP/PS1 double‐transgenic AD mice were administered a 10‐week course of FLX (10 mg/kg/day) injections. Then, spatial learning and memory were evaluated using a Morris water maze test. Immunohistological staining and an unbiased stereological method were used to estimate the total number of dendritic spine synapses in the hippocampus. We found that FLX significantly shortened the mean escape latencies of the 10‐month‐old mice; reduced the elevated levels of soluble Aβ40, Aβ42, and amyloid plaques in the hippocampus; and prevented the decrease in dendritic spine synapses and in postsynaptic protein PSD‐95 density in the dentate gyrus, CA1/2 and CA3 regions of the hippocampus. Our results indicate that reversing synaptic impairment might be considered a promising therapeutic approach for alleviating the cognitive deficits associated with early AD. Moreover, our results suggest that FLX may be a safe and effective drug for delaying the progress of AD, which might provide a starting point for further research into new preventative measures and treatments for AD.

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“…Recent studies have suggested that some of the currently available antidepressant medications may be effective and well tolerated in PD population [53], and clinical trial data support that antidepressants have the potential to treat AD. Antidepressants are reported to regulate stem cell fate to regenerate neurons in the adult hippocampus and are effective in reducing toxic amyloid peptides and are known to increase neurotrophic factors such as the brain-derived neurotrophic factor (BDNF) [54].…”

Section: Antidepressant Effect Of Genipinmentioning

confidence: 99%

Therapeutic Potential of Genipin in Central Neurodegenerative Diseases

Hölscher

2016

CNS Drugs

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Central neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are one of the biggest health problems worldwide. Currently, there is no cure for these diseases. The Gardenia jasminoides fruit is a common herbal medicine in traditional Chinese medicine (TCM), and a variety of preparations are used as treatments for central nervous system (CNS) diseases. Pharmacokinetic studies suggest genipin is one of the main effective ingredients of G. jasminoides fruit extract (GFE). Accumulated research data show that genipin possesses a range of key pharmacological properties, such as anti-inflammatory, neuroprotective, neurogenic, antidiabetic, and antidepressant effects. Thus, genipin shows therapeutic potential for central neurodegenerative diseases. We review the pharmacological actions of genipin for the treatment of neurodegenerative diseases of the CNS. We also describe the potential mechanisms underlying these effects.

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Antidepressants for neuro-regeneration: from depression to Alzheimer’s disease

Cited by 31 publications

References 129 publications

Long-term Ameliorative Effects of the Antidepressant Fluoxetine Exposure on Cognitive Deficits in 3 × TgAD Mice

Long-term Ameliorative Effects of the Antidepressant Fluoxetine Exposure on Cognitive Deficits in 3 × TgAD Mice

Fluoxetine delays the cognitive function decline and synaptic changes in a transgenic mouse model of early Alzheimer's disease

Therapeutic Potential of Genipin in Central Neurodegenerative Diseases

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