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Melissa J. Alldred

Researcher at Nathan Kline Institute for Psychiatric Research

Publications -  45
Citations -  2904

Melissa J. Alldred is an academic researcher from Nathan Kline Institute for Psychiatric Research. The author has contributed to research in topics: Basal forebrain & Cholinergic neuron. The author has an hindex of 24, co-authored 43 publications receiving 2365 citations. Previous affiliations of Melissa J. Alldred include Pennsylvania State University & New York University.

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Sex- and brain region-specific acceleration of β-amyloidogenesis following behavioral stress in a mouse model of Alzheimer's disease

TL;DR: The results suggest that the higher prevalence of sporadic AD in women may be attributable to the vulnerability of female brains to stressful events, which alter APP processing to favor the β-amyloidogenesis through the transcriptional and translational upregulation of BACE1 combined with elevations in its substrate APP.
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Mitovesicles are a novel population of extracellular vesicles of mitochondrial origin altered in Down syndrome.

TL;DR: Using a high-resolution density gradient separation of extracellular vesicles (EVs) isolated from murine and human DS and diploid control brains, this paper identified and characterized a previously unknown population of double-membraned EVs containing multiple mitochondrial proteins distinct from previously described EV subtypes, including microvesicles and exosomes.
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Enhanced exosome secretion in Down syndrome brain - a protective mechanism to alleviate neuronal endosomal abnormalities

TL;DR: It is found that exosome secretion is enhanced in the brains of DS patients and a mouse model of the disease, and by DS fibroblasts, and increased levels of the tetraspanin CD63, a regulator ofExosome biogenesis, were observed in DS brains, suggesting the upregulation of exosomes represents a potential therapeutic goal for neurodegenerative disorders with endosomal pathology.
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Gene expression levels assessed by CA1 pyramidal neuron and regional hippocampal dissections in Alzheimer's disease.

TL;DR: Single population studies of specific neurons and intrinsic circuits will likely yield informative gene expression profile data that may be subthreshold and/or underrepresented in regional studies with an admixture of cell types.
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Apolipoprotein E4 genotype compromises brain exosome production.

TL;DR: Using human and mouse tissue, Peng et al. report that APOE4 reduces brain exosome production and release, which may be the initial event in endosomal-lysosome-exosomal alterations contributing to neuronal vulnerability and neurodegenerative risk in APoe4-carriers.