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alzheimers prevention

Daiqiang Liu, Yaqun Zhou, Yawen Peng, Peng Su, Zheng Li, Qiaoqiao Xu, Ye Tu, Xuebi Tian, Hui Yang, Zhen Wu, Wei Mei, Feng Gao
Morphine tolerance remains an intractable problem, which hinders its prolonged use in clinical practice. Endoplasmic reticulum (ER) stress has been proved to play a fundamental role in the pathogenesis of Alzheimer's disease, diabetes, atherosclerosis, cancer, etc. In this study, we provide the first direct evidence that ER stress may be a significant driver of morphine tolerance. Binding immunoglobulin protein (BiP), the ER stress marker, was significantly upregulated in neurons in spinal dorsal horn in rats being treated with morphine for 7 days...
2018: Frontiers in Molecular Neuroscience
Nancy R Stallings, Melissa A O'Neal, Jie Hu, Ege T Kavalali, Ilya Bezprozvanny, James S Malter
Early-stage Alzheimer's disease is characterized by the loss of dendritic spines in the neocortex of the brain. This phenomenon precedes tau pathology, plaque formation, and neurodegeneration and likely contributes to synaptic loss, memory impairment, and behavioral changes in patients. Studies suggest that dendritic spine loss is induced by soluble, multimeric amyloid-β (Aβ42 ), which, through postsynaptic signaling, activates the protein phosphatase calcineurin. We investigated how calcineurin caused spine pathology and found that the cis-trans prolyl isomerase Pin1 was a critical downstream target of Aβ42 -calcineurin signaling...
March 20, 2018: Science Signaling
Tanusree Sen, Pampa Saha, Nilkantha Sen
Acetylation of the microtubule-associated protein tau promotes its polymerization into neurofibrillary tangles that are implicated in the pathology of Alzheimer's disease (AD). The gaseous neurotransmitter nitric oxide (NO) regulates cell signaling through the nitrosylation of proteins. We found that NO production and tau acetylation at Lys280 occurred in the brain tissue in mice and in cultured mouse cortical neurons in response to exposure to amyloid-β1-42 (Aβ1-42 ), a peptide that is also implicated in AD...
March 20, 2018: Science Signaling
Kolla Rajasekhar, Kapilkumar Mehta, Thimmaiah Govindaraju
Amyloid beta (Aβ) aggregation is the key trait responsible for the pathological devastation caused by Alzheimer's disease (AD). Among the various pathways of multifaceted toxicity exhibited by Aβ aggregates in neuronal cells, generation of reactive oxygen species (ROS) by Aβ-CuII complex and mitochondrial damage are prominent. Aβ interferes with mitochondrial transport channels, causing mitochondrial dysfunction. Herein, we present nontoxic hybrid multifunctional modulators (HMMs, TGR86-88) developed by integrating the structural and functional features of the metal chelating aggregation modulator, clioquinol (Clq) and the antioxidant epigallocatechin gallate (EGCG)...
March 20, 2018: ACS Chemical Neuroscience
Hsin-Hua Li, Chih-Li Lin, Chien-Ning Huang
A growing body of evidence suggests that disruption of the homeostasis of lipid metabolism affects the pathogenesis of Alzheimer's disease (AD). In particular, dysregulation of cholesterol homeostasis in the brain has been reported to considerably increase the risk of developing AD. Thus, dysregulation of lipid homeostasis may increase the amyloid β (Aβ) levels by affecting amyloid precursor protein (APP) cleavage, which is the most important risk factor involved in the pathogenesis of AD. Previous research demonstrated that Aβ can trigger neuronal insulin resistance, which plays an important role in response to Aβ-induced neurotoxicity in AD...
February 2018: Neural Regeneration Research
Yongming Pan, Jianqin Xu, Cheng Chen, Fangming Chen, Ping Jin, Keyan Zhu, Chenyue W Hu, Mengmeng You, Minli Chen, Fuliang Hu
Alzheimer's disease (AD) is the most common form of dementia characterized by aggregation of amyloid β (Aβ) and neuronal loss. One of the risk factors for AD is high cholesterol levels, which are known to promote Aβ deposition. Previous studies have shown that royal jelly (RJ), a product of worker bees, has potential neuroprotective effects and can attenuate Aβ toxicity. However, little is known about how RJ regulates Aβ formation and its effects on cholesterol levels and neuronal metabolic activities...
2018: Frontiers in Aging Neuroscience
Francesca Pistollato, Ruben Calderón Iglesias, Roberto Ruiz, Silvia Aparicio, Jorge Crespo, Luis Dzul Lopez, Piera Pia Manna, Francesca Giampieri, Maurizio Battino
Ample epidemiological evidence suggests a strong correlation among diet, lifestyle factors and the onset and consolidation of dementia and Alzheimer's disease (AD). It has been demonstrated that AD, diabetes, obesity, insulin resistance, and cardiovascular disease are strongly interconnected pathologies. Preventive strategies and nutritional interventions seem to be promising approaches to delay neurocognitive decline and reduce the risk of AD and other non-psychiatric co-morbidities. In this regard, healthy dietary patterns, characterized by high intake of plant-based foods, probiotics, antioxidants, soy beans, nuts, and omega-3 polyunsaturated fatty acids, and a low intake of saturated fats, animal-derived proteins, and refined sugars, have been shown to decrease the risk of neurocognitive impairments and eventually the onset of AD...
March 16, 2018: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Yoko Hirata, Chika Yamada, Yuki Ito, Shotaro Yamamoto, Haruna Nagase, Kentaro Oh-Hashi, Kazutoshi Kiuchi, Hiromi Suzuki, Makoto Sawada, Kyoji Furuta
The current medical and surgical therapies for neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease offer symptomatic relief but do not provide a cure. Thus, small synthetic compounds that protect neuronal cells from degeneration are critically needed to prevent and treat these. Oxidative stress has been implicated in various pathophysiological conditions, including neurodegenerative diseases. In a search for neuroprotective agents against oxidative stress using the murine hippocampal HT22 cell line, we found a novel oxindole compound, GIF-0726-r, which prevented oxidative stress-induced cell death, including glutamate-induced oxytosis and erastin-induced ferroptosis...
March 15, 2018: Neuropharmacology
Yue Cao, Christian Hölscher, Meng-Ming Hu, Ting Wang, Fang Zhao, Yu Bai, Jun Zhang, Mei-Na Wu, Jin-Shun Qi
Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there is no cure. The early primary symptom of AD is the decline of memory ability, which gradually develops into complete dementia. Type 2 diabetes mellitus (T2DM) is an important risk factor of AD; and mimetics of the incretin hormone GLP-1 developed to treat diabetes are being tested as a novel therapeutic strategy for AD. In the present study, we reported for the first time the neuroprotective effects of a novel GLP-1/GIP dual agonist DA5-CH that activates the incretin hormone GLP-1 and GIP receptors in the APP/PS1 transgenic AD mouse model...
March 15, 2018: European Journal of Pharmacology
Varda Shoshan-Barmatz, Edna Nahon-Crystal, Anna Shteinfer-Kuzmine, Rajeev Gupta
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. Although an accumulation of brain amyloid-β (Aβ) peptide and hyperphosphorylated tau protein have been implicated in the pathogenesis of AD, the etiology of the disease remains unclear. Mitochondrial dysfunction has been identified as an early event in AD pathogenesis and is reflected by reduced metabolism, disruption of Ca2+ homeostasis, and increased levels of reactive oxygen species, lipid peroxidation, and apoptosis. The focus of this review is the involvement of mitochondrial dysfunction in AD, and specifically, the role of the voltage-dependent anion channel 1 (VDAC1), which has been linked to AD pathogenesis...
March 15, 2018: Pharmacological Research: the Official Journal of the Italian Pharmacological Society
Aishat T Bakre, Ruoling Chen, Ranjit Khutan, Li Wei, Tina Smith, Gordon Qin, Isaac M Danat, Weiju Zhou, Peter Schofield, Angela Clifford, Jiaji Wang, Arpana Verma, Cuilin Zhang, Jindong Ni
OBJECTIVE: To assess the association of fish consumption with risk of dementia and its dose-response relationship, and investigate variations in the association among low-, middle- and high-income countries. DESIGN: A new community-based cross-sectional study and a systematic literature review. Settings Urban and rural communities in China; population-based studies systematically searched from worldwide literature. SUBJECTS: Chinese adults aged ≥60 years in six provinces (n 6981) took part in a household health survey of dementia prevalence and risk factors...
March 19, 2018: Public Health Nutrition
John R Best, Janice J Eng, Jennifer C Davis, Robin Hsiung, Peter A Hall, Laura E Middleton, Peter Graf, Charles H Goldsmith, Teresa Liu-Ambrose
INTRODUCTION: Cerebrovascular disease-such as stroke-is the second most common cause of dementia (ie, vascular dementia). Specifically, a stroke increases one's risk for dementia by a factor of two. Thus, stroke survivors represent a target population in need of intervention strategies to promote cognitive function and prevent dementia. The current standard of care in stroke rehabilitation does not adequately address the significant cognitive consequences of stroke, especially for those who are in the chronic phase (ie, >12 months since an index stroke)...
March 17, 2018: BMJ Open
Sarang Kim, Mitchell McMaster, Susan Torres, Kay L Cox, Nicola Lautenschlager, George W Rebok, Dimity Pond, Catherine D'Este, Ian McRae, Nicolas Cherbuin, Kaarin J Anstey
INTRODUCTION: It has been estimated that a 10%-25% reduction in seven key risk factors could potentially prevent 1.1-3.0 million Alzheimer's disease cases globally. In addition, as dementia is preceded by more subtle cognitive deficits which have substantial social and economic impact, effective preventative interventions would likely have more extensive benefits. The current study evaluates in primary care a multidomain risk-reduction intervention targeting adults with high risk of developing dementia...
March 17, 2018: BMJ Open
Andrea K H Stavoe, Erika L F Holzbaur
Neurons are long-lived and highly polarized cells that depend on autophagy to maintain cellular homeostasis. The robust, constitutive biogenesis of autophagosomes in the distal axon occurs via a conserved pathway that is required to maintain functional synapses and prevent axon degeneration. Autophagosomes are formed de novo at the axon terminal in a stepwise assembly process, engulfing mitochondrial fragments, aggregated proteins, and bulk cytosol in what appears to be a nonselective uptake mechanism. Following formation, autophagosomes fuse with late endosomes/lysosomes and then are rapidly and efficiently transported along the axon toward the soma, driven by the microtubule motor cytoplasmic dynein...
March 13, 2018: Neuroscience Letters
Qinghui Cheng, Zhi-Wen Hu, Katelynne E Doherty, Yuto J Tobin-Miyaji, Wei Qiang
Disruption of the synaptic plasma membrane (SPM) induced by the aggregation of β-amyloid (Aβ) peptides has been considered as a potential mechanism for the neurotoxicity of Aβ in Alzheimer's disease (AD). However, the molecular basis of such membrane disruption process remains unclear, mainly because of the severe systematic heterogeneity problem that prevents the high-resolution studies. Our previous studies using a two-component phosphatidylcholine (PC)/phosphatidylglycerol (PG) model liposome showed the presence of Aβ-induced membrane disruptions that were either on the pathway or off the pathway of fibril formation...
March 13, 2018: Biochimica et Biophysica Acta
Lucia Panzella, Thomas Eidenberger, Alessandra Napolitano
Black sesame pigment (BSP) represents a low cost, easily accessible material of plant origin exhibiting marked antioxidant and heavy metal-binding properties with potential as a food supplement. We report herein the inhibitory properties of the potentially bioaccessible fraction of BSP following simulated gastrointestinal digestion against key enzymes involved in Alzheimer's disease (AD). HPLC analysis indicated that BSP is transformed under the pH conditions mimicking the intestinal environment and the most abundant of the released compounds was identified as vanillic acid...
March 16, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Alessandro Micarelli, Andrea Viziano, David Della-Morte, Ivan Augimeri, Marco Alessandrini
OBJECTIVE: Considering the altered multisensory signal compensation during senescence, the aim of the present study was to evaluate the integration rearrangements in unilateral vestibular hypofunction (UVH) during age-related cognitive decline. STUDY DESIGN: Cross-sectional study. SETTING: Longitudinal cohort study unit and of University tertiary referral center. PATIENTS: Older UVH individuals ≥ 55 years with Mild Cognitive Impairment (MCI) or Alzheimer Disease (AD) and matched UVH control group with age-appropriate cognitive function...
March 15, 2018: Otology & Neurotology
Anat Elmann, Alona Telerman, Rivka Ofir, Yoel Kashman, Orly Lazarov
Alzheimer's disease (AD) is the most prevalent cause of dementia in adults. Current available drugs for AD transiently alleviate some of the symptoms, but do not modify the disease mechanism or cure it. Therefore, new drugs are desperately needed. Key contributors to AD are amyloid beta (Aβ)- and reactive oxygen species (ROS)-induced cytotoxicities. Plant-derived substances have been shown to affect various potential targets in various diseases including AD. Therefore, phytochemicals which can protect neuronal cells against these insults might help in preventing and treating this disease...
March 15, 2018: Journal of Natural Medicines
Hwan-Hee Kim, Nam-Hae Jung
[Purpose] In this study, we investigated the effects of combining exercise with a cognitive-enhancement group program on cognition and depression in a group of community-dwelling elderly people. [Subjects and Methods] The study's subjects consisted of 30 community-dwelling elderly people of both genders, whose average age was 78 years. They participated in a program of physical exercise combined with a cognitive-enhancement group training program. This consisted of sessions lasting 60 minutes that took place once a week over 3 months...
February 2018: Journal of Physical Therapy Science
Xueying Wang, Ksenia V Kastanenka, Michal Arbel-Ornath, Caitlin Commins, Akira Kuzuya, Amanda J Lariviere, Grant A Krafft, Franz Hefti, Jasna Jerecic, Brian J Bacskai
Soluble amyloid β oligomers (AβOs) are widely recognized neurotoxins that trigger aberrant signaling in specific subsets of neurons, leading to accumulated neuronal damage and memory disorders in Alzheimer's disease (AD). One of the profound downstream consequences of AβO-triggered events is dysregulation of cytosolic calcium concentration ([Ca2+ ]i ), which has been implicated in synaptic failure, cytoskeletal abnormalities, and eventually neuronal death. We have developed an in vitro/in vivo drug screening assay to evaluate putative AβO-blocking candidates by measuring AβO-induced real-time changes in [Ca2+ ]i ...
March 15, 2018: Scientific Reports
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