How much caffeine is your doctor prescribing? Or is your doctor doing NOTHING about your chances of getting dementia/Alzheimers? Don't do caffeine on your own, you know how dangerous drinking and eating is without a doctors prescription. And you don't know the quantities needed.
1. A documented 33% dementia chance post-stroke from an Australian study? May 2012.
2. Then this study came out and seems to have a range from 17-66%. December 2013.
3. A 20% chance in this research. July 2013.
Beneficial effects of caffeine in a transgenic model of Alzheimer's disease-like tau pathology
Article Info
To view the full text, please login as a subscribed user or purchase a subscription. Click here to view the full text on ScienceDirect.
Fig. 1
Concentrations of caffeine and its metabolites in plasma and brains of
chronically-treated animals. (A) Plasma and brain concentrations of caffeine and
its metabolites (paraxanthine, theobromine, and theophylline) assessed using
LC/MS. Caffeine is the main component found in the brain. (B) Brain:plasma ratio
calculated from data given in (A) ratio is close to 1 for caffeine and is
significantly lower for metabolites. Results are expressed as means ± SEM. *
p < 0.05, ** p < 0.01, *** p < 0.001 versus
caffeine using 1W-ANOVA followed by a post hoc Fisher LSD test, n = 11/group.
Results are given as average of pooled data from WT and Tau transgenic mice.
Abbreviations: ANOVA, analysis of variance; LSD, least significant difference;
SEM, standard error of the mean; WT, wild type.
Fig. 2
Caffeine prevents development of spatial memory impairments in THY-Tau22
mice. (A) Learning phase of the Morris Water Maze task. No difference is
observed between groups during the learning phase using path length calculations
following 2-way ANOVA. (B) Velocity is not modified regardless of groups
following 1-way ANOVA followed by a post hoc Fisher LSD test. (C) Probe test
performed 72 hours after the last day of learning. Results are expressed as
means ± SEM of the averaged percent of total time spent in target quadrant (T)
versus nontarget quadrants (NT). Data demonstrate that WT animals exhibit a
significantly preference for target quadrant while THY-Tau22 mice treated with
water did not. THY-Tau22 mice treated with caffeine significantly exhibit a
preference for target quadrant as observed for WT animals. Results are expressed
as means ± SEM. ** p < 0.01 versus Target, using Student t test;
# p < 0.05 versus WT H2O using 1 way-ANOVA,
n = 10–15/group. Abbreviations: ANOVA, analysis of variance; LSD, least
significant difference; SEM, standard error of the mean; WT, wild
type.
Fig. 3
Caffeine reduces tau phosphorylation and tau fragments in THY-Tau22 mice. (A)
Western blot analysis of tau phosphorylation in THY-Tau22 mice treated with
water or caffeine using antibodies targeting physiological (pSer214, pSer396,
pSer404) and pathologic (pThr212/Ser214, pSer422) tau epitopes. We observe a
significant decrease of phosphorylation of Thr212/Ser214, Ser396, and Ser422
epitopes as well as an increase of dephosphorylated tau using Tau1 antibody.
Moreover, caffeine reduces tau fragments (f-Cter and f-Nter) concomitantly with
an increased total tau levels (Cter and Nter). (B) Quantifications were
performed over total tau levels (Cter). Total tau levels were quantified versus
GAPDH, used as loading control. Results are expressed as means ± SEM. THY-Tau22
H2O versus THY-Tau22 caffeine: * p < 0.05, ** p
< 0.01 using Student t test, n = 5–7/group. Abbreviation: SEM,
standard error of the mean.
Fig. 4
Impact of caffeine on hippocampal tau kinases and PP2AC. Western blot
analysis was performed using antibodies raised against total and/or
phosphorylated forms of several tau kinases and PP2AC. Results indicate
increased pErk and cdk5 in caffeine-treated animals together with an
upregulation of PP2AC. Phospho-epitopes were quantified versus total form of
respective protein. Total expressions were quantified versus GAPDH. Results are
expressed as means percentage ± SEM of untreated animals. * p <
0.05, ** p < 0.01 versus nontreated animals, using Student
t test, n = 5–7/group. Abbreviation: SEM, standard error of the
mean.
Fig. 5
Caffeine modulates hippocampal neuroinflammation and oxidative stress markers
in THY-Tau22 mice. qPCR analysis of hippocampal neuroinflammatory and oxidative
stress markers. CD68, CD45, and TLR2 are innate immunity markers, GFAP is a
marker for astrocytes; CCL4, CCL5, and TNFα are cytokines. Nrf2 is a
transcription factor involved in the brain's antioxidant response. MnSOD
catalyzes dismutation of superoxide anion and EAAT3 is a neuronal cysteine
transporter important for de novo glutathione synthesis. All markers display
increased levels in water-treated THY-Tau22 mice compared with WT animals.
Caffeine treatment significantly reduced levels of CD45, TLR2, CCL4, TNFα, Nrf2,
MnSOD, and EAAT3 in THY-Tau22 mice. Results are expressed as means ± SEM. *
p < 0.05, ** p < 0.01, *** p < 0.001 versus
WT H2O; # p < 0.05, ## p
< 0.01, ### p < 0.001 versus THY-Tau22 H2O
using 1 way-ANOVA followed by a post hoc Fisher LSD test, n = 6–10/group.
Abbreviations: ANOVA, analysis of variance; LSD, least significant difference;
qPCR, quantitative polymerase chain reaction; SEM, standard error of the
mean.
No comments:
Post a Comment