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    Alzheimer’s disease tagged posts

    Genetic Variations that Boost PKC enzyme contribute to Alzheimer’s disease

    May 10, 2016, Categories  Biology/Biotechnology, Health/Medical

    One Alzheimer's-associated mutation in the PKC protein leads to a cavity that enhances its activity. Credit: UC San Diego Health

    One Alzheimer’s-associated mutation in the PKC protein leads to a cavity that enhances its activity. Credit: UC San Diego Health

    Researchers found Protein Kinase C (PKC) alpha is necessary for amyloid beta to damage neuronal connections. They also identified genetic variations that enhance PKC alpha activity in patients with Alzheimer’s disease. The study may present a new therapeutic target for the disease. “Until recently, it was thought that PKC helped cells survive, and that too much PKC activity led to cancer. Based on that assumption, many companies tested PKC inhibitors as drugs to treat cancer, but they didn’t work,” said Prof Alexandra Newton, PhD, UC SD School of Medicine.

    “Instead, we recently found that the opposite is true...

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    Gene linked to Alzheimer’s disease Impairs Memory by Disrupting brain’s ‘Playback System’

    May 7, 2016, Categories  Biology/Biotechnology, Health/Medical

    Mice with apoE4 had fewer ripples than mice with the normal apoE3 protein, and they had less slow gamma activity during the ripples. Based on these results, the scientists questioned whether these differences in activity affected the ability to form and replay memories. Image is for illustrative purposes only. Image is credited to Andrews-Zwiling Y. et al./Journal of Neuroscience, and is adapted from the Gladstone Institute video.

    Mice with apoE4 had fewer ripples than mice with the normal apoE3 protein, and they had less slow gamma activity during the ripples. Based on these results, the scientists questioned whether these differences in activity affected the ability to form and replay memories. Image is for illustrative purposes only. Image is credited to Andrews-Zwiling Y. et al./Journal of Neuroscience, and is adapted from the Gladstone Institute video.

    Scientists at the Gladstone Institutes have discovered how the major genetic risk factor for Alzheimer’s disease causes memory impairment. A specific type of brain activity important for memory replay is disrupted in mice with the E4 version of the apolipoprotein E (apoE4) gene, which may interfere with memory formation...

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    Experimental Alzheimer’s Drug Reverses Genetic changes thought to spur the disease

    May 3, 2016, Categories  Biology/Biotechnology, Health/Medical

    After treatment with riluzole, the brains of old rats showed more of a transporter molecule that removes excess glutamate, (green fluorescence, right) as compared to untreated rats (left). Credit: Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology at The Rockefeller University/Molecular Psychiatry

    After treatment with riluzole, the brains of old rats showed more of a transporter molecule that removes excess glutamate, (green fluorescence, right) as compared to untreated rats (left). Credit: Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology at The Rockefeller University/Molecular Psychiatry

    In new research a drug, riluzole, is capable of reversing key genetic changes associated with these conditions. “In aging and Alzheimer’s, the chemical signal glutamate can accumulate between neurons, damaging the circuitry,” Pereira says. “When we treated rats with riluzole, we saw a suite of changes. Perhaps most significantly, expression of molecules responsible for clearing excess glutamate returned to more youthful levels...

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    Early Abnormalities of Alzheimer’s disease: It takes 2 proteins to tango

    April 20, 2016, Categories  Biology/Biotechnology, Health/Medical

    Synergistic effect between [18F]florbetapir SUVR and CSF p-tau drives [18F]FDG uptake decline in limbic regions. Statistical parametric maps, after correcting for multiple comparisons (false discovery rate corrected at P<0.001), overlaid in a structural MRI scan, reveal areas in which 24-month [18F]FDG uptake decline occurs as a function of the synergistic interaction between baseline [18F]florbetapir SUVR and CSF p-tau measurements. Significant interactive effects were observed in the basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices. The analysis was corrected for age, gender and APOE ε4 status. CSF, cerebrospinal fluid; [18F]FDG, [18F]fluorodeoxyglucose; MRI, magnetic resonance imaging; p-tau, phosphorylated tau; SUVR, standardized uptake value ratio.

    Synergistic effect between [18F]florbetapir SUVR and CSF p-tau drives [18F]FDG uptake decline in limbic regions. Statistical parametric maps, after correcting for multiple comparisons (false discovery rate corrected at P<0.001), overlaid in a structural MRI scan, reveal areas in which 24-month [18F]FDG uptake decline occurs as a function of the synergistic interaction between baseline [18F]florbetapir SUVR and CSF p-tau measurements. Significant interactive effects were observed in the basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices. The analysis was corrected for age, gender and APOE ε4 status...

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