Anchors away - Of plaques and pathology in prion disease

Article Abstract:

Transgenic mice are studied to view the procedure of prion propagation, in which a diseased form of the prion protein called PrP(super Sc) forces the normal form of the protein PrP(super C) to convert to a diseased version. It is increasingly accepted that formation of plaques as a result of this conversion are not considered relevant to the pathogenesis of Alzheimer's disease and hence, it is the activity of protofibrils which should be cancelled.

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Tangles and neurodegenerative disease: A surprising twist

Article Abstract:

Researchers address the evaluation of the potential neurotoxicity of neurofibrillary tangles and provide surprising and encouraging data relevant to the goal of clinically reversing the ravages of Dr. Alois Alzheimer disease and related demintias. They engineered mice to express a mutant form of the tau gene, known to cause fronto-temporal dementia, so they could turn the gene on and off by exposing the mice to doxycycline.

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Association between microdeletion and microduplication at 16p11.2 and autism

Article Abstract:

A study to examine the genetic contribution of chromosomal abnormalities to autism, a heritable developmental disorder is conducted. Results indicate that a region of chromosome 16p11.2 influences susceptibility to autism when it is either deleted or duplicated.

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