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https://www.readbyqxmd.com/read/28634681/microtubule-affinity-regulating-kinases-are-potential-druggable-targets-for-alzheimer-s-disease
#1
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
#2
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
#3
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
#4
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
https://www.readbyqxmd.com/read/28628597/integrating-health-promotion-into-physical-therapy-practice-to-improve-brain-health-and-prevent-alzheimer-disease
#5
Ellen McGough, Neva Kirk-Sanchez, Teresa Liu-Ambrose
BACKGROUND AND PURPOSE: Alzheimer disease is the most common cause of dementia, and brain pathology appears years before symptoms are evident. Primary prevention through health promotion can incorporate lifestyle improvement across the lifespan. Risk factor assessment and identifying markers of disease might also trigger preventive measures needed for high-risk individuals and groups. SUMMARY OF KEY POINTS: Many potential risk factors are modifiable through exercise, and may be responsive to early intervention strategies to reduce the downward slope toward disability...
July 2017: Journal of Neurologic Physical Therapy: JNPT
https://www.readbyqxmd.com/read/28626809/epidermal-growth-factor-prevents-apoe4-induced-cognitive-and-cerebrovascular-deficits-in-female-mice
#6
Riya Thomas, Alan W J Morris, Leon M Tai
Cerebrovascular dysfunction is re-emerging as a major component of aging, and may contribute to the risk of developing Alzheimer's disease (AD). Two important risk factors for cerebrovascular dysfunction are APOE and female sex, which are primarily researched in the context of high amyloid-β (Aβ) levels as found in AD. However, APOE4 and sex modulate Aβ-independent pathways that may induce cerebrovascular dysfunction as a downstream consequence. Therefore, testing the activity of factors that target cerebrovascular dysfunction in Aβ-independent models that incorporate APOE4 and female sex is crucial...
June 2017: Heliyon
https://www.readbyqxmd.com/read/28626387/the-case-for-abandoning-therapeutic-chelation-of-copper-ions-in-alzheimer-s-disease
#7
REVIEW
Simon C Drew
The "therapeutic chelation" approach to treating Alzheimer's disease (AD) evolved from the metals hypothesis, with the premise that small molecules can be designed to prevent transition metal-induced amyloid deposition and oxidative stress within the AD brain. Over more than 20 years, countless in vitro studies have been devoted to characterizing metal binding, its effect on Aβ aggregation, ROS production, and in vitro toxicity. Despite a lack of evidence for any clinical benefit, the conjecture that therapeutic chelation is an effective approach for treating AD remains widespread...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28626017/amyloid-beta-peptide-is-needed-for-cgmp-induced-long-term-potentiation-and-memory
#8
Agostino Palmeri, Roberta Ricciarelli, Walter Gulisano, Daniela Rivera, Claudia Rebosio, Elisa Calcagno, Maria Rosaria Tropea, Silvia Conti, Utpal Das, Subhojit Roy, Maria A Pronzato, Ottavio Arancio, Ernesto Fedele, Daniela Puzzo
High levels of amyloid-beta peptide (Aβ) have been related to Alzheimer's disease pathogenesis. However, in the healthy brain, low physiologically relevant concentrations of Aβ are necessary for long-term potentiation (LTP) and memory. Because cGMP plays a key role in these processes, here we investigated whether the cyclic nucleotide cGMP influences Aβ levels and function during LTP and memory. We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors (PDE5-Is) sildenafil and vardenafil induces a parallel release of Aβ due to a change in the approximation of amyloid precursor protein (APP) and the β-site APP cleaving enzyme 1 (BACE1)...
June 16, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28625569/synaptic-dysfunction-in-alzheimer-s-disease-from-the-role-of-amyloid-%C3%AE-peptide-to-the-%C3%AE-secretase-adam10
#9
Stefano Musardo, Elena Marcello
Alzheimer's disease (AD) is emerging as the most prevalent and socially disruptive illness of aging populations as more people live long enough to become affected. Although AD is placing a considerable and increasing burden on patients, caregivers and society, it represents the largest unmet medical need in neurology, because it is currently incurable. In the last few years, the amyloid hypothesis, which points to amyloid β-peptide (Aβ) as the initiating factor in AD, had a central role in the development of therapeutic strategies for AD...
June 15, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28624365/o-glcnacylation-of-amyloid-%C3%AE-precursor-protein-at-threonine-576-residue-regulates-trafficking-and-processing
#10
Yoon Sun Chun, Oh-Hoon Kwon, Sungkwon Chung
The pathological hallmark of Alzheimer's disease (AD) is associated with the accumulation of amyloid-β (Aβ) derived from proteolytic processing of amyloid-β precursor protein (APP). APP undergoes post-translational modification including N- and O-glycosylation. O-GlcNAcylation is a novel type of O-glycosylation, mediated by O-GlcNAc transferase attaching O-β-N-acetylglucosamine (O-GlcNAc) to serine/threonine residues of the target proteins. O-GlcNAc is removed by O-GlcNAcase. We have previously reported that increasing O-GlcNAcylated APP using the O-GlcNAcase inhibitor, PUGNAc, increases its trafficking rate to the plasma membrane and decreases its endocytosis rate, resulting in decreased Aβ production...
June 14, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28623460/spreading-of-pathology-in-alzheimer-s-disease
#11
REVIEW
Zhong-Yue Lv, Chen-Chen Tan, Jin-Tai Yu, Lan Tan
The senile plaques (SPs) and neurofibrillary tangles (NFTs) are the two major pathological hallmarks of AD, which are composed of β-amyloid protein and Tau protein. So the β-amyloid protein (Aβ) and Tau oligomers (oTau) are the majority in the pathology of AD. Recently, the spreading of Aβ and oTau in the brain of AD patients has received heated value. In this review, we summarize recent research progress and aim to figure out the spreading mechanism of Aβ and Tau in AD via introduction of the formation, release, uptake, diffusion between different brain regions, and the propagation principle of Aβ and Tau...
June 16, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/28620833/assessment-of-serum-uric-acid-as-risk-factor-for-tauopathies
#12
Tommaso Schirinzi, Giulia Di Lazzaro, Vito Luigi Colona, Paola Imbriani, Mohammad Alwardat, Giulia Maria Sancesario, Alessandro Martorana, Antonio Pisani
Low levels of serum uric acid (UA) are a risk factor for many neurodegenerative diseases but the role of UA in tauopathies has not been yet fully evaluated. In this study, we assessed the risk associated with serum UA levels in a large group of patients with tauopathies, either primary or secondary. The mean serum UA concentrations of 111 patients with tauopathies (TAU), including 41 with progressive supranuclear palsy (PSP), 45 with Alzheimer's disease (AD) and 25 with frontotemporal dementia (FTD) were compared to that of 130 controls (CTL)...
June 15, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/28615163/understanding-mechanisms-and-seeking-cures-for-alzheimer-s-disease-why-we-must-be-extraordinarily-diverse
#13
Madhav Thambisetty
After more than a century since Dr. Alois Alzheimer first described the pathological hallmarks accompanying the defining clinical features of the disease, we have yet to deliver any meaningful disease-modifying treatments to our patients. In this article, we present a rationale for the need to be "extraordinarily diverse" in seeking effective ways to treat or prevent this devastating disease. Our approach is based on applying a systems-biology perspective at the population level, using a diverse array of 'OMICS' methodologies to identify molecular mechanisms associated with well-established AD risk factors including systemic inflammation, obesity and insulin resistance...
June 14, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28610747/cathepsin-b-plays-a-critical-role-in-inducing-alzheimer-s-disease-like-phenotypes-following-chronic-systemic-exposure-to-lipopolysaccharide-from-porphyromonas-gingivalis-in-mice
#14
Zhou Wu, Junjun Ni, Yicong Liu, Jessica L Teeling, Fumiko Takayama, Alex Collcutt, Paul Ibbett, Hiroshi Nakanishi
A number of clinical and experimental studies have revealed a strong association between periodontitis and accelerated cognitive decline in Alzheimer's disease (AD); however, the mechanism of the association is unknown. In the present study, we tested the hypothesis that cathepsin (Cat) B plays a critical role in the initiation of neuroinflammation and neural dysfunction following chronic systemic exposure to lipopolysaccharide from Porphyromonas gingivalis (PgLPS) in mice (1mg/kg, daily, intraperitoneally)...
June 10, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28607171/astrocyte-transforming-growth-factor-beta-1-protects-synapses-against-a%C3%AE-oligomers-in-alzheimer-s-disease-model
#15
Luan Pereira Diniz, Vanessa Tortelli, Isadora Matias, Juliana Morgado, Ana Paula Bérgamo Araujo, Helen M Melo, Gisele S Seixas da Silva, Soniza V Alves-Leon, Jorge M de Souza, Sergio T Ferreira, Fernanda G De Felice, Flávia Carvalho Alcantara Gomes
Alzheimer's disease (AD) is characterized by progressive cognitive decline, increasingly attributed to neuronal dysfunction induced by amyloid-β oligomers (AβOs). Although the impact of AβOs on neurons has been extensively studied, only recently have the possible effects of AβOs on astrocytes begun to be investigated. Given the key roles of astrocytes in synapse formation, plasticity and function, we sought to investigate the impact of AβOs on astrocytes, and to determine if this impact is related to the deleterious actions of AβOs on synapses...
June 12, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28605901/graphite-templated-amyloid-nanostructures-formed-by-a-potential-pentapeptide-inhibitor-for-alzheimer-s-disease-a-combined-study-of-real-time-atomic-force-microscopy-and-molecular-dynamics-simulations
#16
Na Li, Hyunbum Jang, Ming Yuan, Wanrong Li, Xiaolin Yun, Joon Lee, Qiqige Du, Ruth Nussinov, Jiahua Hou, Ratnesh Lal, Feng Zhang
Self-assembly of peptides is closely related to many diseases, including Alzheimer's, Parkinson's, and prion diseases. Understanding the basic mechanism of this assembly is essential for designing ultimate cure and preventive measures. Template-assisted self-assembly (TASA) of peptides on inorganic substrates can provide fundamental understanding of substrate-dependent peptides assemble, including the role of hydrophobic interface on the peptide fibrillization. Here, we have studied the self-assembly process of a potential pentapeptide inhibitor on the surface of highly oriented pyrolytic graphite (HOPG) using real time atomic force microscopy (RT-AFM) as well as molecular dynamics (MD) simulation...
June 12, 2017: Langmuir: the ACS Journal of Surfaces and Colloids
https://www.readbyqxmd.com/read/28603852/unusual-neuropathological-features-and-increased-brain-aluminium-in-a-resident-of-camelford-uk
#17
Andrew King, Claire Troakes, Miren Aizpurua, Ambreen Mirza, Angela Hodges, Safa Al-Sarraj, Christopher Exley
The possible role of aluminium in the pathogenesis of Alzheimer's disease (AD) has been hotly debated over the past few decades. Whereas the so-called "aluminium hypothesis" was popular in the 1970s and 1980s it has gradually fallen out of favour in the past few years possibly following a number of inconclusive and contradictory human environmental/clinical studies. Nevertheless, there have from time to time been reminders in the media of environmental accidents; these have prevented the topic from disappearing completely from public memory...
June 12, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/28603025/the-ampa-receptor-positive-allosteric-modulator-s-47445-rescues-in%C3%A2-vivo-ca3-ca1-long-term-potentiation-and-structural-synaptic-changes-in-old-mice
#18
Albert Giralt, María Ángeles Gómez-Climent, Rafael Alcalá, Sylvie Bretin, Daniel Bertrand, José María Delgado-García, Esther Pérez-Navarro, Jordi Alberch, Agnès Gruart
Positive allosteric modulators of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) are small molecules that decrease deactivation of AMPARs via an allosteric site. These molecules keep the receptor in an active state. Interestingly, this type of modulator has been proposed for treating cognitive decline in ageing, dementias, and Alzheimer's disease (AD). S 47445 (8-cyclopropyl-3-[2-(3-fluorophenyl)ethyl]-7,8-dihydro-3H-[1,3]oxazino[6,5-g][1,2,3]benzotriazine-4,9-dione) is a novel AMPAR positive allosteric modulator (AMPA-PAM)...
June 8, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28602601/association-of-amine-biomarkers-with-incident-dementia-and-alzheimer-s-disease-in-the-framingham-study
#19
Vincent Chouraki, Sarah R Preis, Qiong Yang, Alexa Beiser, Shuo Li, Martin G Larson, Galit Weinstein, Thomas J Wang, Robert E Gerszten, Ramachandran S Vasan, Sudha Seshadri
INTRODUCTION: The identification of novel biomarkers associated with Alzheimer's disease (AD) could provide key biological insights and permit targeted preclinical prevention. We investigated circulating metabolites associated with incident dementia and AD using metabolomics. METHODS: Plasma levels of 217 metabolites were assessed in 2067 dementia-free Framingham Offspring Cohort participants (mean age = 55.9 ± 9.7 years; 52.4% women). We studied their associations with future dementia and AD risk in multivariate Cox models...
June 8, 2017: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
https://www.readbyqxmd.com/read/28600952/time-course-of-tau-toxicity-and-pharmacologic-prevention-in-a-cell%C3%A2-model-of-tauopathy
#20
Marcus Pickhardt, Jacek Biernat, Sabrina Hübschmann, Frank J A Dennissen, Thomas Timm, Annukka Aho, Eva-Maria Mandelkow, Eckhard Mandelkow
The aggregation of Tau protein is a hallmark of neurodegenerative diseases including Alzheimer's disease. Previously, we generated a cell model of tauopathy based on the 4-repeat domain with the FTDP-17 mutation ΔK280 (Tau(4RDΔK)) which is expressed in a regulatable fashion (tet-on). The deletion variant ΔK280 is highly amyloidogenic and forms fibrous aggregates in neuroblastoma N2a cells staining with the reporter dye Thioflavin S. The aggregation of Tau(4RDΔK) is toxic, contrary to wildtype or anti-aggregant variants of the protein...
May 3, 2017: Neurobiology of Aging
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