Alzheimer’s disease tagged posts

DNA Vaccine Protects against Toxic Proteins linked to Alzheimer’s

DNA vaccine protects against toxic proteins linked to Alzheimer's

UT Southwestern researchers have developed a DNA vaccine that helps the body protect against toxic proteins associated with Alzheimer’s disease. These images show amyloid plaque in the mouse brain using plasma containing anti-amyloid antibody from large mammals immunized with the vaccine. Credit: UT Southwestern

A new DNA vaccine when delivered to the skin prompts an immune response that produces antibodies to protect against toxic proteins associated with Alzheimer’s disease – without triggering severe brain swelling that earlier antibody treatments caused in some patients. Two studies from the Peter O’Donnell Jr. Brain Institute demonstrate in animals how a vaccine containing DNA of the toxic beta-amyloid protein elicits a different immune response that may be safe for humans...

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Is Soda bad for your Brain? (And is Diet Soda worse?)

New research correlates sugary drinks—as well as diet soda—to smaller brain volume and memory deficits. Photo by RapidEye/iStock

Both sugary, diet drinks correlated with accelerated brain aging. Researchers using data from the Framingham Heart Study (FHS) found that people who drink sugary beverages frequently are more likely to have poorer memory, smaller overall brain volume, and a significantly smaller hippocampus. A follow-up study found that people who drank diet soda daily were almost 3X as likely to develop stroke and dementia when compared to those who did not.

Researchers are quick to point out that these findings, which appear separately in the journals Alzheimer’s & Dementia and Stroke, demonstrate correlation but not cause-and-effect...

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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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