Alzheimer’s disease tagged posts

Never before seen Images of Early stage Alzheimer’s disease

Images that predate the formation of toxic clumps of beta-amyloid, the protein believed to be at the root of Alzheimer’s disease, have now been captured by researchers. Credit: Illustration: Per Uvdal

Images that predate the formation of toxic clumps of beta-amyloid, the protein believed to be at the root of Alzheimer’s disease, have now been captured by researchers. Credit: Illustration: Per Uvdal

MAX IV synchrotron in Lund, Sweden – the strongest of its kind in the world – has been used to produce images that predate the formation of toxic clumps of beta-amyloid, the protein believed to be at the root of Alzheimer’s disease. The unique images appear to contradict a previously unchallenged consensus. Instead of attempting to eliminate beta-amyloid plaques, the researchers now suggest stabilizing the protein.

It is a long-held belief in the scientific community that the beta-amyloid plaques appear almost instantaneously. Hence the term “popcorn plaques...

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Combating Iron in the Brain: Researchers find anti-aging micromolecule

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members 2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri. Three different clusters were isolated (pri-mir-29 1, 2, 3) encoding four different mature members miR-29a, b, d, e. In red, seed sequence is reported, single nucleotide differences in blue. b Age-dependent expression of miR-29 primary transcripts (Pri-miR-29-1, 2, 3) in the brain of N. furzeri. The relative expression was evaluated by RT-qPCR, data were normalized on TATA binding protein (TBP), pri-miR-29-2 results much more expressed than the other clusters and shows a clear age-dependent up-regulation (1 way ANOVA with post-test for trend: R = 0.5285 P < 0.0001, n = 4 animals for age group). c Correlation of miR-29 with its predicted targets. Blue bars show the distribution of Pearson’s correlation coefficients between miR-29a and its predicted target. Light-blue bars show the distribution of correlation values extracted from a bootstrap (P = 10–14, Kolmogorov–Smirnoff). d, e Pri-miR-29-2 expression pattern in N. furzeri brain. d Pri-miR-29-2 signal (red) and HuC/D expression (green) in the optic tectum (TeO). Pri-miR-29-2 shows a nuclear staining and a co-localization with neuronal marker HuC/D along the periventricular gray zone (PGZ), white arrows show neurons in the optic tectum (TeO) negative for pri-miR-29-2. Scale bar = 50 μm. Cerebellum overview picture (e) shows a clear and strong expression of pri-miR-29-2 just in the granular cell layer (GCL), it is instead absent in the Purkinje cell (white arrow) and molecular layer (ML). Scale bar 100 μm

1. Schematic model of miR-29 action in brain aging. During aging an accumulation of iron in neurons occurs. This induces expression of miR-29 that in turn represses expression of IRP-2 thereby limiting iron uptake. This mechanism counteracts aging-related damages. MiR-29 may also counteract effects aging-related phenotypes by additional mechanisms, for example modulation of pro-apoptotic BCL-2 family members
2. MiR-29 is up-regulated with age in neurons. a Genomic organization of miR-29 family in N. furzeri.

The older we get, our brain ages. Cognitive abilities decline and the risk of developing neurodegenerative diseases like dementia, Alzheimer’s and Parkinson’s disease or having a stroke steadily increases...

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Roots of Alzheimer’s disease can extend as far back as the Womb

Vitamin A deficiency increased the production of plaques in the brain of mice.

Vitamin A deficiency increased the production of plaques in the brains of mice.

Vitamin A deficiency could ‘program’ brain tissue. Biochemical reactions that cause Alzheimer’s disease could begin in the womb or just after birth if the fetus or newborn does not get enough vitamin A, according to new research from the University of British Columbia. These new findings, based on studies of genetically-engineered mice, also demonstrate that Vit A supplement given to newborns with low levels of vitamin A could be effective in slowing the degenerative brain disease.

“Our study clearly shows that marginal deficiency of vitamin A, even as early as in pregnancy, has a detrimental effect on brain development and has long-lasting effect that may facilitate Alzheimer’s disease in later life,” said Dr...

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In Alzheimer’s, excess Tau protein damages brain’s GPS

This is a grid cell from the entorhinal cortex (EC) of the mouse brain, firing repeatedly and uniformly in a grid-like pattern. When a mouse moves through its environment, grid cells are activated, with each cell representing a specific location. This creates a triangular coordinate system that allows for spatial navigation. Several grid cells create a triangular coordinate system that allows for spatial navigation. The accumulation of tau protein in the brain of a mouse model of Alzheimer's disease was shown to disrupt the function of grid cells, causing problems with navigation. The findings explains why Alzheimer's patients tend to wander and get lost. Credit: Lab of Karen Duff, PhD, Columbia University Medical Center

This is a grid cell from the entorhinal cortex (EC) of the mouse brain, firing repeatedly and uniformly in a grid-like pattern. When a mouse moves through its environment, grid cells are activated, with each cell representing a specific location. This creates a triangular coordinate system that allows for spatial navigation. Several grid cells create a triangular coordinate system that allows for spatial navigation. The accumulation of tau protein in the brain of a mouse model of Alzheimer’s disease was shown to disrupt the function of grid cells, causing problems with navigation. The findings explains why Alzheimer’s patients tend to wander and get lost. Credit: Lab of Karen Duff, PhD, Columbia University Medical Center

Finding may explain why many Alzheimer’s disease patients wander...

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