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Your search keyword '"Angulo, S. L."' showing total 2 results
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2 results on '"Angulo, S. L."'

1. Genetic underpinnings in Alzheimer’s disease: a review

Author

Moustafa, A. A., Hassan, M., Hewedi, D., Garami, J., Alashwal, H., Zaki, N., Seo, S. Y., Cutsuridis, V., Angulo, S. L., Hewedi, E., Natesh, J. Y., Herzallah, M. M., Frydecka, D., Misiak, B., Salama, M., Mohamed, W., El Haj, M., Hornbeger, M., Moustafa, A. A., Hassan, M., Hewedi, D., Garami, J., Alashwal, H., Zaki, N., Seo, S. Y., Cutsuridis, V., Angulo, S. L., Hewedi, E., Natesh, J. Y., Herzallah, M. M., Frydecka, D., Misiak, B., Salama, M., Mohamed, W., El Haj, M., and Hornbeger, M.

Abstract

In this review, we discuss the genetic etiologies of Alzheimer’s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein (APP) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP) and late-onset (apolipoprotein E, ApoE) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.

2. Tau and amyloid-related pathologies in the entorhinal cortex have divergent effects in the hippocampal circuit.

Author

Angulo SL, Orman R, Neymotin SA, Liu L, Buitrago L, Cepeda-Prado E, Stefanov D, Lytton WW, Stewart M, Small SA, Duff KE, and Moreno H

Subjects
Amyloid beta-Protein Precursor genetics, Animals, Computer Simulation, Entorhinal Cortex pathology, Female, Hippocampus pathology, Humans, Male, Membrane Potentials physiology, Mice, Inbred C57BL, Mice, Transgenic, Models, Neurological, Mutation, Neural Pathways metabolism, Neural Pathways pathology, Neurons pathology, Patch-Clamp Techniques, Synapses metabolism, Synapses pathology, Synaptic Transmission physiology, Tissue Culture Techniques, tau Proteins genetics, Amyloid beta-Protein Precursor metabolism, Entorhinal Cortex metabolism, Hippocampus metabolism, Neurons metabolism, tau Proteins metabolism
Abstract

The entorhinal cortex (EC) is affected early in Alzheimer's disease, an illness defined by a co-occurrence of tau and amyloid-related pathologies. How the co-occurrence of these pathologies in the EC affects the hippocampal circuit remains unknown. Here we address this question by performing electrophysiological analyses of the EC circuit in mice that express mutant human amyloid precursor protein (hAPP) or tau (hTau), or both in the EC. We show that the alterations in the hippocampal circuit are divergent, with hAPP increasing but hTau decreasing neuronal/circuit excitability. Most importantly, mice co-expressing hAPP and hTau show that hTau has a dominant effect, dampening the excitatory effects of hAPP. Additionally, compensatory synaptic downscaling, in response to increased excitability in EC was observed in subicular neurons of hAPP mice. Based on simulations, we propose that EC interneuron pruning can account for both EC hyperexcitability and subicular synaptic downscaling found in mice expressing hAPP., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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