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Nataliya Golovyashkina et al.
Molecular neurodegeneration, 10, 60-60 (2015-11-07)
Dendritic simplification, a key feature of the neurodegenerative triad of Alzheimer's disease (AD) in addition to spine changes and neuron loss, occurs in a region-specific manner. However, it is unknown how changes in dendritic complexity are mediated and how they
Tziona Ben-Gedalya et al.
The EMBO journal, 34(22), 2820-2839 (2015-10-07)
Do different neurodegenerative maladies emanate from the failure of a mutual protein folding mechanism? We have addressed this question by comparing mutational patterns that are linked to the manifestation of distinct neurodegenerative disorders and identified similar neurodegeneration-linked proline substitutions in
Teresa Niccoli et al.
Current biology : CB, 26(17), 2291-2300 (2016-08-16)
Glucose hypometabolism is a prominent feature of the brains of patients with Alzheimer's disease (AD). Disease progression is associated with a reduction in glucose transporters in both neurons and endothelial cells of the blood-brain barrier. However, whether increasing glucose transport
Gunjan Manocha et al.
Current Alzheimer research, 15(12), 1123-1135 (2018-08-03)
Alzheimer's disease (AD) is associated with age-associated central nervous system degeneration and dementia. This decline in the function correlates with deposition of Aβ peptide containing plaques and associated reactive gliosis. The inflammatory phenotype of microglia, in particular, is often considered
Sooah Jang et al.
Psychiatry investigation, 15(2), 205-213 (2018-02-25)
Conventional methods for organotypic hippocampal tissue slice culture (OHSC) have shown several disadvantages or limitations regarding age of animals used, duration of culture and difficulty using neurodegenerative models. Therefore, we tried to establish OHSC from old 3xTg-Alzheimer's disease (AD) mice
Ruth Maron et al.
International journal of molecular sciences, 21(9) (2020-05-10)
The two major proteins involved in Alzheimer's disease (AD) are the amyloid precursor protein (APP) and Tau. Here, we demonstrate that these two proteins can bind to each other. Four possible peptides APP1 (390-412), APP2 (713-730), Tau1 (19-34) and Tau2
Jin-Xiu Pan et al.
Communications biology, 4(1), 1326-1326 (2021-11-27)
Patients with Alzheimer's disease (AD) often have osteoporosis or osteopenia. However, their direct link and relationship remain largely unclear. Previous studies have detected osteoporotic deficits in young adult Tg2576 and TgAPPsweOCN mice, which express APPswe (Swedish mutant) ubiquitously and selectively
Yoon Young Cho et al.
Molecules (Basel, Switzerland), 25(23) (2020-12-02)
Amyloid precursor protein (APP) at the plasma membrane is internalized via endocytosis and delivered to endo/lysosomes, where neurotoxic amyloid-β (Aβ) is produced via β-, γ-secretases. Hence, endocytosis plays a key role in the processing of APP and subsequent Aβ generation.
Mariya V Hrynchak et al.
Frontiers in synaptic neuroscience, 12, 16-16 (2020-05-12)
Alzheimer's disease is regarded as a synaptopathy with a long presymptomatic phase. Soluble, oligomeric amyloid-β (Aβ) is thought to play a causative role in this disease, which eventually leads to cognitive decline. However, most animal studies have employed mice expressing
Kendra L Puig et al.
Journal of Alzheimer's disease : JAD, 44(4), 1263-1278 (2014-11-20)
Alzheimer's disease (AD) is a neurodegenerative disorder histologically characterized by amyloid-β (Aβ) protein accumulation and activation of associated microglia. Although these features are well described in the central nervous system, the process and consequences of Aβ accumulation in the enteric
Angela M Floden et al.
Current Alzheimer research, 17(12), 1133-1144 (2021-01-20)
Beta amyloid (Aβ) peptide containing plaque aggregations in the brain are a hallmark of Alzheimer's Disease (AD). However, Aβ is produced by cell types outside of the brain suggesting that the peptide may serve a broad physiologic purpose. Based upon
Jin Young Shin et al.
Autophagy, 10(1), 32-44 (2013-10-24)
Current evidence suggests a central role for autophagy in Alzheimer disease (AD), and dysfunction in the autophagic system may lead to amyloid-β (Aβ) accumulation. Using in vitro and in vivo AD models, the present study investigated whether mesenchymal stem cells
Loukia Katsouri et al.
Neurobiology of aging, 34(4), 1105-1115 (2012-10-16)
Noradrenergic deficits have been described in the hippocampus and the frontal cortex of Alzheimer's disease brains, which are secondary to locus coeruleus degeneration. Locus coeruleus is the brain stem nucleus responsible for synthesis of noradrenaline and from where all noradrenergic
Ekram Abdel Salam et al.
Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology, 33(1), 13-18 (2014-05-21)
The presence of non-progressive cognitive impairment is recognized as a common feature in a substantial proportion of patients with Duchenne muscular dystrophy (DMD). Concurrently, the amyloid beta peptide (Aβ42) protein has been associated with changes in memory and cognitive functions.
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