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MitoQ inhibits memory loss and neuropathology while extending lifespan in aged mice

mitoq memory alzheimers

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#1 macrohistory

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Posted 18 September 2019 - 11:43 AM


Mol Cell Neurosci. 2019 Sep 12:103409. doi: 10.1016/j.mcn.2019.103409. [Epub ahead of print]

The mitochondria-targeted antioxidant MitoQ inhibits memory loss, neuropathology, and extends lifespan in aged 3xTg-AD mice.
Author information
1 The University of Georgia College of Pharmacy, Department of Pharmaceutical and Biomedical Sciences, 357 Wilson Pharmacy, Athens, GA 30602, USA. Electronic address: mlyoung@uga.edu. 2 The University of Georgia College of Pharmacy, Department of Pharmaceutical and Biomedical Sciences, 357 Wilson Pharmacy, Athens, GA 30602, USA. Electronic address: jlfrankl@uga.edu.
Abstract

Oxidative stress, likely stemming from dysfunctional mitochondria, occurs before major cognitive deficits and neuropathologies become apparent in Alzheimer's disease (AD) patients and in mouse models of the disease. We previously reported that treating 2- to 7-month-old 3xTg-AD mice with the mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-Dimethoxy-2-methyl-3,6-dioxo-1,4-cyclohexadien-1-yl)decyl](triphenyl)phosphonium methanesulfonate), a period when AD-like pathologies first manifest in them, prevents AD-like symptoms from developing. To elucidate further a role for mitochondria-derived oxidative stress in AD progression, we examined the ability of MitoQ to inhibit AD-like pathologies in these mice at an age in which cognitive and neuropathological symptoms have fully developed. 3xTg-AD female mice received MitoQ in their drinking water for five months beginning at twelve months after birth. Untreated 18-month-old 3xTg-AD mice exhibited significant learning deficits and extensive AD-like neuropathologies. MitoQ-treated mice showed improved memory retention compared to untreated 3xTg-AD mice as well as reduced brain oxidative stress, synapse loss, astrogliosis, microglial cell proliferation, Aβ accumulation, caspase activation, and tau hyperphosphorylation. Additionally, MitoQ treatment significantly increased the abbreviated lifespan of the 3xTg-AD mice. These findings support a role for the involvement of mitochondria-derived oxidative stress in the etiology of AD and suggest that mitochondria-targeted antioxidants may lessen symptoms in AD patients.

 


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#2 Mind

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Posted 18 September 2019 - 03:13 PM

....in mice

 

However, MitoQ seems to be one of most studied supplements on the market. Most of the research has been positive for health.


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#3 tolerant

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Posted 19 October 2019 - 11:19 AM

Does anyone know what the shelf life of MitoQ is? I bought a bottle about 10 months ago but didn't end up taking it because I was alerted of this: https://www.ncbi.nlm...les/PMC5880956/

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#4 aribadabar

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Posted 20 October 2019 - 07:34 PM

Does anyone know what the shelf life of MitoQ is? I bought a bottle about 10 months ago but didn't end up taking it because I was alerted of this: https://www.ncbi.nlm...les/PMC5880956/

 

The bottle should list an expiry date. Add 6-12 months after that and you are still fine to use them.


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#5 tolerant

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Posted 03 November 2019 - 10:44 AM

The bottle should list an expiry date. Add 6-12 months after that and you are still fine to use them.

 

Thank you. It is really stupid of me not to have looked at the expiry date on the bottle. Just shows the cognitive issues which I thought MitoQ could possibly address. I took one tablet daily for two days to see if there would be any positive acute effect that would allow me to to research the kidney toxicity issue. Unfortunately, I didn't feel anything from it.


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