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Alzheimer's prevention

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https://www.readbyqxmd.com/read/28650104/alzheimer-s-disease-and-metabolic-syndrome-a-link-from-oxidative-stress-and-inflammation-to-neurodegeneration
#1
REVIEW
Eduardo Rojas-Gutierrez, Guadalupe Muñoz-Arenas, Samuel Treviño, Blanca Espinosa, Raúl Chavez, Karla Rojas, Gonzalo Flores, Alfonso Díaz, Jorge Guevara
Alzheimer's disease (AD) is the most common cause of dementia and one of the most important causes of morbidity and mortality among the aging population. AD diagnosis is made post-mortem, and the two pathologic hallmarks, particularly evident in the end stages of the illness, are amyloid plaques and neurofibrillary tangles (NFT). Currently, there is no curative treatment for AD. Additionally, there is a strong relation between oxidative stress, metabolic syndrome (MetS) and AD. The high levels of circulating lipids and glucose imbalances amplify lipid peroxidation that gradually diminishes the antioxidant systems, causing high levels of oxidative metabolism that affects cell structure, leading to neuronal damage...
June 26, 2017: Synapse
https://www.readbyqxmd.com/read/28649597/early-diagnosis-of-mild-cognitive-impairment-and-alzheimer-s-disease-based-on-salivary-lactoferrin
#2
Eva Carro, Fernando Bartolomé, Félix Bermejo-Pareja, Alberto Villarejo-Galende, José Antonio Molina, Pablo Ortiz, Miguel Calero, Alberto Rabano, José Luis Cantero, Gorka Orive
INTRODUCTION: The Alzheimer's disease (AD) process is likely initiated many years before clinical onset. Biomarkers of preclinical disease are critical for the development of disease-modifying or even preventative therapies. Current biomarkers for early disease, including cerebrospinal fluid tau and amyloid β (Aβ) levels, structural and functional magnetic resonance imaging, and the use of brain amyloid imaging, are limited because they are very invasive or expensive. Noninvasive biomarkers may be a more accessible alternative, but none can currently detect preclinical AD with the required sensitivity and specificity...
2017: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/28648388/heterozygous-knockout-of-cytosolic-phospholipase-a2%C3%AE-attenuates-alzheimer-s-disease-pathology-in-app-ps1-transgenic-mice
#3
Baoxi Qu, Yunhua Gong, Jassica M Gill, Kimbra Kenney, Ramon Diaz-Arrastia
Cytosolic Phospholipase A2α (cPLA2α) is a key enzyme in regulation of inflammation process and neuromembrane homeostasis, both of which are critical in pathogenesis of Alzheimer's diseases. By hybride APP/PS1 Tg-AD mice with cPLA2α knockout mice, three lines of APP/PS1 Tg-AD mice were produced with genotypes of cPLA2α +/+, cPLA2α +/- and cPLA2α-/-. Compared to cPLA2α +/+ Tg-AD mice, the amyloid plaque formation was significantly downregulated in the brain of cPLA2α+/- Tg-AD mice, but not in cPLA2α -/- Tg-AD mice...
June 22, 2017: Brain Research
https://www.readbyqxmd.com/read/28647555/normalizing-the-gene-dosage-of-dyrk1a-in-a-mouse-model-of-down-syndrome-rescues-several-alzheimer-s-disease-phenotypes
#4
Susana García-Cerro, Noemí Rueda, Verónica Vidal, Sara Lantigua, Carmen Martínez-Cué
The intellectual disability that characterizes Down syndrome (DS) is primarily caused by prenatal changes in central nervous system growth and differentiation. However, in later life stages, the cognitive abilities of DS individuals progressively decline due to accelerated aging and the development of Alzheimer's disease (AD) neuropathology. The AD neuropathology in DS has been related to the overexpression of several genes encoded by Hsa21 including DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A), which encodes a protein kinase that performs crucial functions in the regulation of multiple signaling pathways that contribute to normal brain development and adult brain physiology...
June 21, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28647031/cover-story-towards-a-preventive-treatment-of-alzheimer-s-disease-with-multi-functional-liposomes
#5
EDITORIAL
Kinam Park
No abstract text is available yet for this article.
July 28, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28646794/dexibuprofen-prevents-neurodegeneration-and-cognitive-decline-in-appswe-ps1de9-through-multiple-signaling-pathways
#6
Miren Ettcheto, Elena Sánchez-López, Laura Pons, Oriol Busquets, Jordi Olloquequi, Carlos Beas-Zarate, Merce Pallas, Maria Luisa García, Carme Auladell, Jaume Folch, Antoni Camins
The aim of the present study is to elucidate the neuronal pathways associated to NSAIDs causing a reduction of the risk and progression of Alzheimer's disease. The research was developed administering the active enantiomer of ibuprofen, dexibuprofen (DXI), in order to reduce associated gastric toxicity. DXI was administered from three to six-month-old female APPswe/PS1dE9 mice as a model of familial Alzheimer's disease. DXI treatment reduced the activation of glial cells and the cytokine release involved in the neurodegenerative process, especially TNFα...
June 15, 2017: Redox Biology
https://www.readbyqxmd.com/read/28645294/3-5-4-trihydroxy-6-7-3-trimethoxyflavone-protects-against-beta-amyloid-induced-neurotoxicity-through-antioxidative-activity-and-interference-with-cell-signaling
#7
Alona Telerman, Rivka Ofir, Yoel Kashman, Anat Elmann
BACKGROUND: Alzheimer's disease is a neurodegenerative disease, characterized by progressive decline in memory and cognitive functions, that results from loss of neurons in the brain. Amyloid beta (Aβ) protein and oxidative stress are major contributors to Alzheimer's disease, therefore, protecting neuronal cells against Aβ-induced toxicity and oxidative stress might form an effective approach for treatment of this disease. 3,5,4'-trihydroxy-6,7,3'-trimethoxyflavone (TTF) is a flavonoid we have purified from the plant Achillea fragrantissima; and the present study examined, for the first time, the effects of this compound on Aβ-toxicity to neuronal cells...
June 23, 2017: BMC Complementary and Alternative Medicine
https://www.readbyqxmd.com/read/28643167/microbiome-probiotics-and-neurodegenerative-diseases-deciphering-the-gut-brain-axis
#8
REVIEW
Susan Westfall, Nikita Lomis, Imen Kahouli, Si Yuan Dia, Surya Pratap Singh, Satya Prakash
The gut microbiota is essential to health and has recently become a target for live bacterial cell biotherapies for various chronic diseases including metabolic syndrome, diabetes, obesity and neurodegenerative disease. Probiotic biotherapies are known to create a healthy gut environment by balancing bacterial populations and promoting their favorable metabolic action. The microbiota and its respective metabolites communicate to the host through a series of biochemical and functional links thereby affecting host homeostasis and health...
June 22, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28642806/the-efficacy-of-epigallocatechin-3-gallate-green-tea-in-the-treatment-of-alzheimer-s-disease-an-overview-of-pre-clinical-studies-and-translational-perspectives-in-clinical-practice
#9
REVIEW
Marco Cascella, Sabrina Bimonte, Maria Rosaria Muzio, Vincenzo Schiavone, Arturo Cuomo
Alzheimer's disease (AD) is a neurodegenerative disorder and the most common form of dementia characterized by cognitive and memory impairment. One of the mechanism involved in the pathogenesis of AD, is the oxidative stress being involved in AD's development and progression. In addition, several studies proved that chronic viral infections, mainly induced by Human herpesvirus 1 (HHV-1), Cytomegalovirus (CMV), Human herpesvirus 2 (HHV-2), and Hepatitis C virus (HCV) could be responsible for AD's neuropathology...
2017: Infectious Agents and Cancer
https://www.readbyqxmd.com/read/28642635/virtual-screening-following-rational-drug-design-based-approach-for-introducing-new-anti-amyloid-beta-aggregation-agent
#10
Garshasb Rigi, Mohammad Vala Ashdar Nakhaei, Hoda Eidipour, Arshia Najimi, Fahimeh Tajik, Niloufar Taher, Kamran Yarahmadi
Amyloid β (Aβ) sheets aggregations is the main reason of Alzheimer disease. The interacting areas between monomers are residue number 38 to 42. Inhibition of interaction between Aβ molecules prevents plaque formation. In the present study, we have performed a high-throughput virtual screening among ZINC database and top 1000 hits were checked again regarding binding affinity by AutoDock software. Top 4 successive second step screening hits was considered for drug design purpose against aggregation site of Aβ molecules...
2017: Bioinformation
https://www.readbyqxmd.com/read/28640179/engagement-in-pleasant-leisure-activities-and-blood-pressure-a-5-year-longitudinal-study-in-alzheimer-s-caregivers
#11
Brent T Mausbach, Rosa Romero-Moreno, Taylor Bos, Roland von Känel, Michael G Ziegler, Matthew A Allison, Paul J Mills, Joel E Dimsdale, Sonia Ancoli-Israel, Andrés Losada, María Márquez-González, Thomas L Patterson, Igor Grant
OBJECTIVE: Elevated blood pressure is a significant public health concern, particularly given its association with cardiovascular disease risk, including stroke. Caring for a loved one with Alzheimer's disease has been associated with physical health morbidity, including higher blood pressure. Engagement in adaptive coping strategies may help prevent blood pressure elevation in this population. This 5-year longitudinal study examined whether greater participation in pleasant leisure activities was associated with reduced blood pressure in caregivers...
May 31, 2017: Psychosomatic Medicine
https://www.readbyqxmd.com/read/28639617/gene-therapy-for-spinomuscular-atrophy-a-biomedical-advance-a-missed-opportunity-for-more-equitable-drug-pricing
#12
T Friedmann
An experimental approach for gene therapy of spinomuscular atrophy has been reported to prevent development of the neuromuscular features of this lethal and previously untreatable disorder. The approach involves treatment of patients suffering from SMN1-associated infantile form of the disease with a splice-switching antisense oligonucleotide (ASO) that corrects aberrant splicing of the nearly identical SMN2 gene to allow the generation of functional SMN protein, thereby mitigating the development of the disease...
June 22, 2017: Gene Therapy
https://www.readbyqxmd.com/read/28639593/synaptic-roles-of-cyclin-dependent-kinase-5-its-implications-in-epilepsy
#13
REVIEW
Aparna Banerjee Dixit, Jyotirmoy Banerjee, Manjari Tripathi, Chitra Sarkar, P Sarat Chandra
There is an urgent need to understand the molecular mechanisms underlying epilepsy to find novel prognostic/diagnostic biomarkers to prevent epilepsy patients at risk. Cyclin-dependent kinase 5 (CDK5) is involved in multiple neuronal functions and plays a crucial role in maintaining homeostatic synaptic plasticity by regulating intracellular signalling cascades at synapses. CDK5 deregulation is shown to be associated with various neurodegenerative diseases such as Alzheimer's disease. The association between chronic loss of CDK5 and seizures has been reported in animal models of epilepsy...
February 2017: Indian Journal of Medical Research
https://www.readbyqxmd.com/read/28637867/full-length-cellular-beta-secretase-has-a-trimeric-subunit-stoichiometry-and-its-sulfur-rich-transmembrane-interaction-site-modulates-cytosolic-copper-compartmentalization
#14
Filip Liebsch, Mark R P Aurousseau, Tobias Bethge, Hugo McGuire, Silvia Scolari, Andreas Herrmann, Rikard Blunck, Derek Bowie, Gerd Multhaup
The beta-secretase (BACE1) initiates processing of the amyloid precursor protein (APP) into Aβ peptides, which have been implicated as central players in the pathology of Alzheimer disease. BACE1 has been described as a copper-binding protein and its oligomeric state as being monomeric, dimeric, and/or multimeric, but the native cellular stoichiometry has remained elusive. Here, by using single-molecule fluorescence and in vitro cross-linking experiments with photo-activatable unnatural amino acids, we show that full-length BACE1, independently of its subcellular localization, exists as trimers in human cells...
June 21, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28637402/antioxidant-skq1-alleviates-signs-of-alzheimer-s-disease-like-pathology-in-old-oxys-rats-by-reversing-mitochondrial-deterioration
#15
Nataliya G Kolosova, Mikhail A Tyumentsev, Natalia A Muraleva, Elena Kiseleva, Anton O Vitovtov, Natalia A Stefanova
BACKGROUND: Mitochondrial dysfunction is called the missing link between brain aging and Alzheimer's disease (AD), the most common type of age-related dementia worldwide. Among the most advanced and promising of approaches to prevention or slowing of AD are therapeutic strategies targeting mitochondria. OBJECTIVE: Mitochondria-targeted antioxidant SkQ1 can suppress the development of AD signs, but its therapeutic potential in AD at clinical stages is currently unknown...
June 21, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28637354/essential-dietary-bioactive-lipids-in-neuroinflammatory-diseases
#16
M Valeria Catani, Valeria Gasperi, Tiziana Bisogno, Mauro Maccarrone
Under physiological conditions, neurons and glia are in a healthy, redox-balanced environment; when injury perturbs this equilibrium, a neuroinflammatory state is established by activated microglia that triggers pro-inflammatory responses and alters the oxidant/antioxidant balance, thus leading to neuronal loss and neurodegeneration. In neurodegenerative diseases (such as Alzheimer's disease, Parkinson's disease, amyothrophic lateral sclerosis, and multiple sclerosis), the brain is in a constitutively self-sustaining cycle of inflammation and oxidative stress that prompts and amplifies brain damage...
June 22, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28634681/microtubule-affinity-regulating-kinases-are-potential-druggable-targets-for-alzheimer-s-disease
#17
REVIEW
Narendran Annadurai, Khushboo Agrawal, Petr Džubák, Marián Hajdúch, Viswanath Das
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects normal functions of the brain. Currently, AD is one of the leading causes of death in developed countries and the only one of the top ten diseases without a means to prevent, cure, or significantly slow down its progression. Therefore, newer therapeutic concepts are urgently needed to improve survival and the quality of life of AD patients. Microtubule affinity-regulating kinases (MARKs) regulate tau-microtubule binding and play a crucial role in neurons...
June 20, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28633663/targeting-psychologic-stress-signaling-pathways-in-alzheimer-s-disease
#18
REVIEW
Hunter S Futch, Cara L Croft, Van Q Truong, Eric G Krause, Todd E Golde
Alzheimer's Disease (AD) is the most prevalent progressive neurodegenerative disease; to date, no AD therapy has proven effective in delaying or preventing the disease course. In the search for novel therapeutic targets in AD, it has been shown that increased chronic psychologic stress is associated with AD risk. Subsequently, biologic pathways underlying psychologic stress have been identified and shown to be able to exacerbate AD relevant pathologies. In this review, we summarize the literature relevant to the association between psychologic stress and AD, focusing on studies investigating the effects of stress paradigms on transgenic mouse models of Amyloid-β (Aβ) and tau pathologies...
June 21, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28633568/the-potential-inhibitory-effect-of-%C3%AE-casein-on-the-aggregation-and-deposition-of-a%C3%AE-1-42-fibrils-in-alzheimer-s-disease-insight-from-in-vitro-and-in-silico-studies
#19
Sedighehsadat Hojati, Arezou Ghahghaei, Milad Lagzian
Aβ1-40 and Aβ1-42 have been shown to be the main components of the amyloid plaques found in the extracellular environment of neurons in Alzheimer's disease. β-Casein, a milk protein, has been shown to display a remarkable chaperone ability in preventing the aggregation of proteins. In this study, the ability of β-casein to suppress the amyloid fibril formation of Aβ1-42 has been examined through in vitro studies and molecular docking simulation. The results demonstrate the inhibitory effect of β-casein on fibril formation in Aβ1-42, in a concentration dependent manner, suggesting that the chaperone binds to the Aβ1-42 and prevents amyloid fibril formation...
June 20, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/28630497/chronic-treatment-with-a-smart-antioxidative-nanoparticle-for-inhibition-of-amyloid-plaque-propagation-in-tg2576-mouse-model-of-alzheimer-s-disease
#20
Phetcharat Boonruamkaew, Pennapa Chonpathompikunlert, Long Binh Vong, Sho Sakaue, Yasushi Tomidokoro, Kazuhiro Ishii, Akira Tamaoka, Yukio Nagasaki
The present study aimed to assess whether our newly developed redox nanoparticle (RNP(N)) that has antioxidant potential decreases Aβ levels or prevents Aβ aggregation associated with oxidative stress. The transgenic Tg2576 Alzheimer's disease (AD) mice were used to investigate the effect of chronic ad libitum drinking of RNP(N) solution for 6 months, including memory and learning functions, antioxidant activity, and amyloid plaque aggregation. The results showed that RNP(N)-treated mice had significantly attenuated cognitive deficits of both spatial and non-spatial memories, reduced oxidative stress of lipid peroxide, and DNA oxidation...
June 19, 2017: Scientific Reports
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