Alzheimer’s disease tagged posts

Antibody, Aducanumab, reduces harmful brain Amyloid Plaques in Alzheimer’s patients

Biogen Alzheimer's paper Figure 1 | Amyloid plaque reduction with aducanumab: example amyloid PET images at baseline and week 54. Individuals were chosen based on visual impression and SUVR change relative to average one-year response for each treatment group (n = 40, 32, 30 and 32, respectively). Axial slice shows anatomical regions in posterior brain putatively relatedto AD pathology. SUVR, standard uptake value ratio.

Amyloid plaque reduction with aducanumab: example amyloid PET images at baseline and week 54. Axial slice shows anatomical regions in posterior brain putatively related to Alzheimer’s disease pathology

The researchers furthermore demonstrated in an early stage clinical study that, after 1 year of treatment with Aducanumab, cognitive decline could be significantly slowed in antibody-treated patients as opposed to the placebo group. Although the causes of Alzheimer’s disease are still unknown, it is clear that the disease commences with progressive amyloid deposition in the brains of affected persons between 10 to 15 years before the emergence of initial clinical symptoms such as memory loss...

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Study suggests ‘Use it or Lose it’ to defend against Memory Loss

Auriel Willette with images of brain scans

Auriel Willette used data from brain scans and memory tests to track the progression of Alzheimer’s disease. Photo by Blake Lanser

Iowa State University researchers have identified a protein essential for building memories that appears to predict the progression of memory loss and brain atrophy in Alzheimer’s patients. The findings also suggest there is a link between brain activity and the presence of the protein neuronal pentraxin-2, or NPTX2. The research, published in the journal Brain, Behavior and Immunity, found a correlation between higher levels of NPTX2 and better memory and more brain volume. Lower levels of the protein were associated with diminished memory and less volume.

“NPTX2 seems to exert a protective effect,” Swanson said...

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New Link found between Diabetes, Alzheimer’s disease

Defective neuronal insulin sensitivity in PLB4 mice. (a) Simplified schematic showing insulin signalling. (b) Representative immunoblots of insulin-related markers in brain lysates from 8-month-old PLB4 and WT mice and (c) quantification of their relative expression. White bars, WT mice; black bars, PLB4 mice. Data are means + SEM normalised to WT values. *p < 0.05

Defective neuronal insulin sensitivity in PLB4 mice. (a) Simplified schematic showing insulin signalling. (b) Representative immunoblots of insulin-related markers in brain lysates from 8-month-old PLB4 and WT mice and (c) quantification of their relative expression. White bars, WT mice; black bars, PLB4 mice. Data are means + SEM normalised to WT values. *p < 0.05

Drugs used to treat diabetes could also be used to treat Alzheimer’s disease, and vice versa, according to new research from the University of Aberdeen. This is also the first study of its kind to show that Alzheimer’s disease can lead to diabetes, as opposed to diabetes occurring first as was previously thought...

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Alzheimer’s Researchers find Clues to Toxic forms of Amyloid beta

Fibrils formed by the aggregation of the amyloid beta protein can be seen in these transmission electron microscope images, which show differences in fibril morphology between the normal protein (above) and an altered protein with one amino acid replaced by its mirror image. The altered protein also forms fibrils more slowly and is more toxic to cells. (Image credit: Warner et al., CEJ 2016)

Fibrils formed by the aggregation of the amyloid beta protein can be seen in these transmission electron microscope images, which show differences in fibril morphology between the normal protein (above) and an altered protein with one amino acid replaced by its mirror image. The altered protein also forms fibrils more slowly and is more toxic to cells. (Image credit: Warner et al., CEJ 2016)

Subtle change to amyloid beta protein affects its aggregation behavior, stabilizes an intermediate form with enhanced toxicity. Much of the research on Alzheimer’s disease has focused on the amyloid beta protein, which clumps together into sticky fibrils that form deposits in the brains of people with the disease...

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