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    Thursday, 9 March 2017

    Caffeine Safeguards Against Dementia

    Researchers at Indiana University have identified a compound in coffee and tea that boosts neuroprotective function. The compound, found in caffeine, is one of 24 others found to boost an enzyme in the brain that guards against the development of dementia. Called nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2), the enzyme was first discovered through research at IU Bloomington last year. This latest research linking caffeine to NMNAT2 production was published in ScientificReports.

    Neuroprotective enzyme NMNAT2 has a protective effect on the brain, guarding neurons from stress and simultaneously counteracting the negative effects of misfolded proteins by binding to proteins to prevent them from misfolding. These proteins, called tau, become misfolded as product of aging and form in the brain as “plaques.” Misfolded tau proteins have been linked to neurodegenerative disorders – Alzheimer’s, Parkinson’s, Huntington’s and Lou Gehrig’s disease. 

    The same research team responsible for demonstrating the positive effect of caffeine on NMNAT2 production released previous work affirming NMNAT2’s effect on brain function. Lu’s team administered caffeine to specially-bred mice with high levels of misfolded tau and saw improved memory function. Interestingly, the modified mice produced lower levels of NMNAT2.

    Using mice specially-bred to produce low levels of NMNAT2, researchers tested the effects of caffeine on the neuroprotective enzyme. Modified mice were given doses of caffeine or saline (for control). Researchers observed the effects on the mice’s brain function, discovering that those being dosed with caffeine produced the same levels of the enzyme as regular mice. Of the 24 substances found to stimulate the production of NMNAT2, caffeine was the most potent.

    In summation, caffeine was shown to improve memory function and increase the production of the enzyme NMNAT2. This is not the first time that caffeine has been linked to reduced risk of dementia, nor is this the first instance in which it was found to help the formation NMNAT2.

    Over 1,280 pharmacologically active compounds were screened by the research team to observe their influence on the production of NMNAT2 in brain cells. Aside from caffeine, rolipram was the most effective at aiding in the production of the enzyme. Rolipram was used as an antidepressant, but was discontinued in the 1990s. Other brain protecting compounds include ziprasidone, cantharidin, wortmannin and retinoic acid. Furthermore, 13 compounds were found to reduce NMNAT2 production.

    “This work could help advance efforts to develop drugs that increase levels of this enzyme in the brain, creating a chemical ‘blockade’ against the debilitating effects of neurodegenerative disorders,” said Hui-Chen Lu, leader of the study and professor in the Department of Psychological and Brain Sciences at IU Bloomington’s College of Arts and Sciences, in a press release. The team has made major headway towards understanding and preventing neurodegenerative diseases.

    “Increasing our knowledge about the pathways in the brain that appear to naturally cause the decline of this necessary protein is equally as important as identifying compounds that could play a role in future treatment of these debilitating mental disorders.” 

    Jacqui Litvan

    Jacqui Litvan, wielding a bachelor's degree in English, strives to create a world of fantasy amidst the ever-changing landscape of military life. Attempting to become a writer, she fuels herself with coffee (working as a barista) and music (spending free time as a raver).
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