So after learning about the different possible mechanisms that contribute to AD (described briefly below), it made me wondering what type of antioxidant intake research is out there regarding AD. Seems to be a mounting body of evidenced that flavonoids, particularly anthocyanin (responsible for the bright red/purple pigment in foods) maybe beneficial.
Possible mechanisms to produce AD:
1. reduced synthesis of acetylcholine (neurotransmitter)
2. hyperphosporlyation of tau proteins leading to neurofibrillary tangles
3. accumulation of amyloid beta plaques ---seems to be a connection to anthocyanins....
A paper published this past year looked at the affects of mulberry (ME), rich in anthocyanin ---(a flavonoid) on preventing AD in senescence-accelerated mice. Background evidenced indicated that antioxidant-rich berries can positively affect cognition and memory. Specifically, cyanidin-3-O-glycopyranoside (one of the most common anthocyanin) has been identified a "neuroprotective," by decreaseing amyloid beta peptide-medicated cytotoxicity in neurocytes. Other studies found that cyanidin-rich supplements improved lipid oxidation in the brain as well as spatial working memory tests in aged rats (via cAMP-response element).
This study examined 6-month old adult mice from SAMR1 (senescence-resistant) and SAMP8 (senescence-accelerated prone) strains. They found the following:
1. ME significantly improved memory deterioration
2. ME reduced oxidative stress-induced lipid oxidation (via isoprotane reduction)
3. ME improved MAPK cascade via lower levels of p38 and JNK as well as decreased nuclear Nrf2 levels (MAPK regulator), simular to that of the SAMR1 mice (control, not accelerated aging mice)
4. ME reduced the accumulation of amlyoid beta deposits in the hippocampus of the mice feed the extract.
Overall, they found the anthocyanins "promoted age-dependent antioxidant production and reduced oxidative stress-intduced damage."
Food for thought.
Shih P, et al. Antioxidant and cognitive promotion effects of anthocyanin-rich mulberry on senescence-accelerated mice and prevention of Alzheimer's disease. Science Direct. 2010;595-605
Great article, Great Explanation!
ReplyDeleteYour post made me think of some common things college students consume. One prominent drink is COFFEE!
It just popped into my mind because many of us are vigorously studying right now because the semester is winding down…And we drink coffee to stay awake and focused.
So, I decided to look up some articles related to coffee consumption and neurological disorders. I found a review article entitled "Coffee and its Consumption: Benefits and Risks." The article talks about various diseases but because this is neurodegenerative week I will explains parts of the article pertaining to Alzheimer’s Disease (AD).
The authors cite studies related to coffee consumption over a few decades that may delay or reduce the risk of amyloid formation within the brain. They state moderate daily consumption of caffeinated coffee correlated to a decreased expression of Presenilin 1(PS1) and β-secretase (BACE) (Arendash et al. 2006). These enzymes play a significant role in amyloid formation so decreasing the activity and/or expression of these proteins may be a prominent therapeutic route (Fujimoto et al., 2008). Another chemical within coffee that may provide potential benefits is Trigonelline. One particular study using mouse models demonstrates that trigonelline intake corresponded with regeneration of axons and dendrites along with improved memory (via water maze retention tests between control group versus trigonelline injected group) (Tohda et al., 2005).
Aside from these positive correlations listed above, coffee consumption may ameliorate oxidative stress by acting as an anti-oxidant.
Keep in mind that they considered coffee by itself with no cream or sweeteners…
Works cited:
Arendash, G.W., Schleif, W., Rezai-Zadeh, K., Jackson, E.K., Zacharia, L.C., Cracchiolo, J.R., Shippy, D., and Tan, J. (2006). Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain beta-amyloid production. Neuroscience. 142: 941–952
Butt, MS, and MT Sultan. "Coffee and Its Consumption: Benefits and Risks." Critical Reviews in Food Science and Nutrition. 51.4 (2011): 363-73. Print.
(THE REVIEW ARTICLE)
Fujimoto, T., Matsushita, Y., Gouda, H., Yamaotsu, N., and Hirono, S. (2008). In silico multi-filter screening approaches for developing novel β-secretase inhibitors. Bioorg. Med. Chem. Lett. 18: 2771–2775
Tohda, C., Kuboyama, T., and Komatsu, K. (2005). Search for natural products related to regeneration of the neuronal network. Neurosignals.
Good thoughts!
ReplyDeleteCoffee is considered a phenolic acid, a little different than flavonoids.... typically a person consumes ~1/3 of their total phenols from phenolic acid and 2/3 from flavonoids; however heavy coffee drinks will likely consume more phenolic acids than flavonoids. And it's one of the biggest antioxidant "foods" consumed in the U.S.
Coffee might not be so bad.
Tapiero, H. et al. Polyphenols: do they play a role in the prevention of human pathologies. Biomed Pharmacothr. 2001;56:200-7.