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Find video protocols related to scientific articles indexed in Pubmed.
A?38 in the brains of patients with sporadic and familial Alzheimer's disease and transgenic mouse models.
J. Alzheimers Dis.
PUBLISHED: 10-31-2014
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The pathogenesis of Alzheimer's disease (AD) is believed to be closely dependent on deposits of neurotoxic amyloid-? peptides (A?), which become abundantly present throughout the central nervous system in advanced stages of the disease. The different A? peptides existing are generated by subsequent cleavage of the amyloid-? protein precursor (A?PP) and may vary in length and differ at their C-terminus. Despite extensive studies on the most prevalent species A?40 and A?42, A? peptides with other C-termini such as A?38 have not received much attention. In the present study, we used a highly specific and sensitive antibody against A?38 to analyze the distribution of this A? species in cases of sporadic and familial AD, as well as in the brains of a series of established transgenic AD mouse models. We found A?38 to be present as vascular deposits in the brains of the majority of sporadic AD cases, whereas it is largely absent in non-demented control cases. A?38-positive extracellular plaques were virtually limited to familial cases. Interestingly we observed A?38-positive plaques not only among familial cases due to A?PP mutations, but also in cases of familial AD caused by presenilin (PSEN) mutations. Furthermore we demonstrate that A?38 deposits in the form of extracellular plaques are common in several AD transgenic mouse models carrying either only A?PP, or combinations of A?PP, PSEN1, and tau transgenes.
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Axonal degeneration in an Alzheimer mouse model is PS1 gene dose dependent and linked to intraneuronal A? accumulation.
Front Aging Neurosci
PUBLISHED: 01-01-2014
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Abnormalities and impairments in axonal transport are suggested to strongly contribute to the pathological alterations underlying AD. The exact mechanisms leading to axonopathy are currently unclear, but it was recently suggested that APP expression itself triggers axonal degeneration. We used APP transgenic mice and crossed them on a hemi- or homozygous PS1 knock-in background (APP/PS1KI). Depending on the mutant PS1 dosage, we demonstrate a clear aggravation in both plaque-associated and plaque-distant axonal degeneration, despite of an unchanged APP expression level. Amyloid-? (A?) peptides were found to accumulate in axonal swellings as well as in axons and apical dendrites proximate to neurons accumulating intraneuronal A? in their cell bodies. This suggests that A? can be transported within neurites thereby contributing to axonal deficits. In addition, diffuse extracellular A? deposits were observed in the close vicinity of axonal spheroids accumulating intracellular A?, which might be indicative of a local A? release from sites of axonal damage.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.