Antidepressant sertraline increases thioflavin-S and Congo red deposition in APPswe/PSEN1dE9 transgenic mice

Liao, Ming-Hsuan; Lin, Yen-Kuang; Gau, Fong-Ying; Tseng, Chun-Che; Wu, Da-Chih; Hsu, Chu-Yuan; Chung, Kuo-Hsuan; Li, Rung-Chi; Hu, Chaur-Jong; Then, Chee Kin; Shen, Shing-Chuan

doi:10.3389/fphar.2023.1260838

Cited by 2 publications

(2 citation statements)

References 57 publications

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“… 130 , 150 Depression treatments in dementia can also be explored using animal models. The antidepressant sertraline, but not paroxetine, is reported to increase Aβ deposition and gliosis in APP/PS1 mice, 151 consistent with human cohort studies suggesting that antidepressants may increase dementia risk. 152 Exercise, in contrast, can alleviate depressive behaviors in APP/PS1 mice, potentially by altering energy and neurotransmitter metabolism.…”

Section: Social Engagement‐related Modifiable Risk Factorssupporting

confidence: 76%

Experimental laboratory models as tools for understanding modifiable dementia risk

Sinclair,

Canty,

Ziebell

et al. 2024

Alzheimer's & Dementia

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Experimental laboratory research has an important role to play in dementia prevention. Mechanisms underlying modifiable risk factors for dementia are promising targets for dementia prevention but are difficult to investigate in human populations due to technological constraints and confounds. Therefore, controlled laboratory experiments in models such as transgenic rodents, invertebrates and in vitro cultured cells are increasingly used to investigate dementia risk factors and test strategies which target them to prevent dementia. This review provides an overview of experimental research into 15 established and putative modifiable dementia risk factors: less early‐life education, hearing loss, depression, social isolation, life stress, hypertension, obesity, diabetes, physical inactivity, heavy alcohol use, smoking, air pollution, anesthetic exposure, traumatic brain injury, and disordered sleep. It explores how experimental models have been, and can be, used to address questions about modifiable dementia risk and prevention that cannot readily be addressed in human studies.Highlights Modifiable dementia risk factors are promising targets for dementia prevention. Interrogation of mechanisms underlying dementia risk is difficult in human populations. Studies using diverse experimental models are revealing modifiable dementia risk mechanisms. We review experimental research into 15 modifiable dementia risk factors. Laboratory science can contribute uniquely to dementia prevention.

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Section: Social Engagement‐related Modifiable Risk Factorssupporting

confidence: 76%

Experimental laboratory models as tools for understanding modifiable dementia risk

Sinclair,

Canty,

Ziebell

et al. 2024

Alzheimer's & Dementia

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show abstract

“…The observation and image acquisition of plaque deposition in hippocampus and cortex was observed under an optical microscope (Olympus, Tokyo, Japan). 32 …”

Section: Methodsmentioning

confidence: 99%

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

Li,

Sun,

et al. 2024

CNS Neurosci Ther

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BackgroundThis work elucidated the effect of honokiol (HKL) on hippocampal neuronal mitochondrial function in Alzheimer's disease (AD).MethodsAPP/PS1 mice were used as AD mice models and exposed to HKL and 3‐TYP. Morris water maze experiment was performed to appraise cognitive performance of mice. Hippocampal Aβ+ plaque deposition and neuronal survival was evaluated by immunohistochemistry and Nissl staining. Hippocampal neurons were dissociated from C57BL/6 mouse embryos. Hippocampal neuronal AD model was constructed by Aβ oligomers induction and treated with HKL, CsA and 3‐TYP. Neuronal viability and apoptosis were detected by cell counting kit‐8 assay and TUNEL staining. mRFP–eGFP–LC3 assay, MitoSOX Red, dichlorodihydrofluorescein diacetate, and JC‐1 staining were performed to monitor neuronal autophagosomes, mitochondrial reactive oxygen species (ROS), neuronal ROS, and mitochondrial membrane potential. Autophagy‐related proteins were detected by Western blot.ResultsIn AD mice, HKL improved cognitive function, relieved hippocampal Aβ1–42 plaque deposition, promoted hippocampal neuron survival, and activated hippocampal SIRT3 expression and mitochondrial autophagy. These effects of HKL on AD mice were abolished by 3‐TYP treatment. In hippocampal neuronal AD model, HKL increased neuronal activity, attenuated neuronal apoptosis and Aβ aggregation, activated SIRT3 and mitochondrial autophagy, reduced mitochondrial and neuronal ROS, and elevated mitochondrial membrane potential. CsA treatment and 3‐TYP treatment abrogated the protection of HKL on hippocampal neuronal AD model. The promotion of mitochondrial autophagy by HKL in hippocampal neuronal AD model was counteracted by 3‐TYP.ConclusionsHKL activates SIRT3‐mediated mitochondrial autophagy to mitigate hippocampal neuronal damage in AD. HKL may be effective in treating AD.

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Antidepressant sertraline increases thioflavin-S and Congo red deposition in APPswe/PSEN1dE9 transgenic mice

Cited by 2 publications

References 57 publications

Experimental laboratory models as tools for understanding modifiable dementia risk

Experimental laboratory models as tools for understanding modifiable dementia risk

Honokiol relieves hippocampal neuronal damage in Alzheimer's disease by activating the SIRT3‐mediated mitochondrial autophagy

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