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Shuai Zhang, Xueyuan Hu, Wei Guan, Li Luan, Bei Li, Qichao Tang, Honggang Fan
Isoflurane anesthesia has been shown to be responsible for cognitive impairment in Alzheimer's disease (AD) and development of AD in the older age groups. However, the pathogenesis of AD-related cognitive impairments induced by isoflurane anesthesia remains elusive. Thus, this study was designed to investigate the mechanism by which isoflurane anesthesia caused AD-related cognitive impairments. Aged Wistar rats were randomly divided into 6 groups (n = 12), 1 control group (CONT) and 5 isoflurane treated (ISO) groups (ISO 0, ISO 0...
2017: PloS One
J He, L-L Chen, D-K Sun, H-T Wang, J-J Wang, X Zhai
OBJECTIVE: This study examines the relationship between intracranial pressure (ICP) changes after skull injury repair and neurocognitive function before and after the repair. PATIENTS AND METHODS: Sixty patients undergoing skull injury repair participated in the study. A non-invasive detection analyzer was used to detect the ICP 2 days before operation, 10 days after the operation and one month after the operation in all patients. Additionally, the mean cerebral blood flow velocities (MV) in the internal carotid and the medial cerebral arteries were detected using a transcranial Doppler ultrasound (TCD)...
March 2017: European Review for Medical and Pharmacological Sciences
Craig Ritchie, Nadja Smailagic, Anna H Noel-Storr, Obioha Ukoumunne, Emma C Ladds, Steven Martin
BACKGROUND: Research suggests that measurable change in cerebrospinal fluid (CSF) biomarkers occurs years in advance of the onset of clinical symptoms (Beckett 2010). In this review, we aimed to assess the ability of CSF tau biomarkers (t-tau and p-tau) and the CSF tau (t-tau or p-tau)/ABeta ratio to enable the detection of Alzheimer's disease pathology in patients with mild cognitive impairment (MCI). These biomarkers have been proposed as important in new criteria for Alzheimer's disease dementia that incorporate biomarker abnormalities...
March 22, 2017: Cochrane Database of Systematic Reviews
Prasad Tammineni, Qian Cai
Macroautophagy/autophagy plays a key role in cellular quality control by eliminating protein aggregates and damaged organelles, which is essential for the maintenance of neuronal homeostasis. Defective autophagy has been implicated in the pathogenesis of Alzheimer disease (AD). In AD brains, autophagic vacuoles (AVs) accumulate massively within dystrophic neurites. This raises a fundamental question as to whether impaired autophagic clearance contributes to AD-associated autophagic stress. We recently revealed that AD neurons display defective retrograde transport and accumulation of amphisomes predominantly in axons and presynaptic terminals...
February 28, 2017: Autophagy
Ta Yuan Chang, Yoshio Yamauchi, Mazahir Hasan, Catherine Cy Chang
Alzheimer's disease [AD] is the most common form of dementia in older adults. Currently, there is no cure for AD. The hallmark of AD is the accumulation of extracellular amyloid plaques composed of amyloid beta peptides [Abeta; especially Abeta1-42], and neurofibrillary tangles, composed of hyper-phosphorylated tau, accompanied with chronic neuroinflammation. Abeta are derived from the amyloid precursor protein APP. The oligomeric form of Abeta is probably the most neurotoxic species; its accumulation eventually forms the insoluble and aggregated amyloid plaques...
March 15, 2017: Journal of Lipid Research
Elisa Conti, Maria Gregori, Isabella Radice, Fulvio Da Re, Denise Grana, Francesca Re, Elisa Salvati, Massimo Masserini, Carlo Ferrarese, Chiara Paola Zoia, Lucio Tremolizzo
The accumulation of extracellular amyloid beta (Abeta42) both in brain and in cerebral vessels characterizes Alzheimer's disease (AD) pathogenesis. Recently, the possibility to functionalize nanoparticles (NPs) surface with Abeta42 binding molecules, making them suitable tools for reducing Abeta42 burden has been shown effective in models of AD. Aim of this work consisted in proving that NPs might be effective in sequestering Abeta42 in biological fluids, such as CSF and plasma. This demonstration is extremely important considering that these Abeta42 pools are in continuum with the brain parenchyma with drainage of Abeta from interstitial brain tissue to blood vessel and plasma...
February 23, 2017: Neurochemistry International
Vito Antonio Baldassarro, Alessandra Marchesini, Luciana Giardino, Laura Calzà
Microvascular dysfunction is considered an integral part of Alzheimer disease (AD) pathogenesis, but the possible relationship between amyloid pathology, microvascular dysfunction and cell death is still unclear. In order to investigate the influence of intraneuronal Abeta (Aβ) accumulation on vulnerability to hypoxia, we isolated primary cortical neurons from Tg2576 (carrying the APPSwe mutation) and Wt fetal mice. We first demonstrated that neurons isolated from Tg2576 new-born mice show an increase in VEGFa mRNA expression and a decrease in the expression of the two VEGF receptors, i...
February 24, 2017: Disease Models & Mechanisms
Brian Murray, Bhanushee Sharma, Georges Belfort
Although the amyloid (abeta peptide, Aβ) hypothesis is 25 years old, is the dominant model of Alzheimer's disease (AD) pathogenesis, and guides the development of potential treatments, it is still controversial. One possible reason is a lack of a mechanistic path from the cleavage products of the amyloid precursor protein (APP) such as soluble Aβ monomer and soluble molecular fragments to the deleterious effects on synaptic form and function. From a review of the recent literature and our own published work including aggregation kinetics and structural morphology, Aβ clearance, molecular simulations, long-term potentiation measurements with inhibition binding, and the binding of a commercial monoclonal antibody, aducanumab, we hypothesize that the N-terminal domains of neurotoxic Aβ oligomers are implicated in causing the disease...
February 10, 2017: ACS Chemical Neuroscience
Junxia Lu, Xing-Qi Dong, Jian-Jun Zhang
Alzheimer's disease (AD) has become the most common neurodegenerative disease. The deposition of amyloid fibrils in the brain is one of the characteristics of AD. The fibrils are composed of amyloid-b peptide (Ab). Ab is produced through a series event of protease cleavage of a transmembrane protein called β-amyloid precursor protein (APP) which is commonly expressed in the brain. The production of Ab and its propensity to aggregation to form oligomers and fibrils are believed to initiate a sequence of events that lead to AD dementia...
February 8, 2017: Protein and Peptide Letters
T Harach, N Marungruang, N Duthilleul, V Cheatham, K D Mc Coy, G Frisoni, J J Neher, F Fåk, M Jucker, T Lasser, T Bolmont
Alzheimer's disease is the most common form of dementia in the western world, however there is no cure available for this devastating neurodegenerative disorder. Despite clinical and experimental evidence implicating the intestinal microbiota in a number of brain disorders, its impact on Alzheimer's disease is not known. To this end we sequenced bacterial 16S rRNA from fecal samples of Aβ precursor protein (APP) transgenic mouse model and found a remarkable shift in the gut microbiota as compared to non-transgenic wild-type mice...
February 8, 2017: Scientific Reports
Tuancheng Feng, Prasad Tammineni, Chanchal Agrawal, Yu Young Jeong, Qian Cai
β-Site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) is the major neuronal β-secretase for amyloid-β generation and is degraded in lysosomes. The autophagy-lysosomal system plays a key role in the maintenance of cellular homeostasis in neurons. Recent studies established that nascent autophagosomes in distal axons move predominantly in the retrograde direction toward the soma, where mature lysosomes are mainly located. However, it remains unknown whether autophagy plays a critical role in regulation of BACE1 trafficking and degradation...
February 3, 2017: Journal of Biological Chemistry
Alexandre Vallée, Yves Lecarpentier
The molecular mechanisms underlying the pathophysiology of Alzheimer's disease (AD) are still not fully understood. In AD, Wnt/beta-catenin signaling has been shown to be downregulated while the peroxisome proliferator-activated receptor (PPAR) gamma (mARN and protein) is upregulated. Certain neurodegenerative diseases share the same Wnt/beta-catenin/PPAR gamma profile, such as bipolar disorder and schizophrenia. Conversely, other NDs share an opposite profile, such as amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, multiple sclerosis, and Friedreich's ataxia...
2016: Frontiers in Neuroscience
William M Pardridge
INTRODUCTION: Therapeutic antibodies are large molecule drugs that do not cross the blood-brain barrier (BBB). Therefore, drug development of therapeutic antibodies for Alzheimer's disease (AD) requires that these molecules be re-engineered to enable BBB delivery. This is possible by joining the therapeutic antibody with a transporter antibody, resulting in the engineering of a BBB-penetrating bispecific antibody (BSA). AREAS COVERED: The manuscript covers transporter antibodies that cross the BBB via receptor-mediated transport systems on the BBB, such as the insulin receptor or transferrin receptor...
September 7, 2016: Expert Opinion on Biological Therapy
Xiaojuan Yang, Yuzhou Yuan, Qiao Niu
OBJECTIVE: To study the effect of aluminum chloride on amyloid precursor protein ( APP ) promoter methylation and the content of amyloid beta-protein (Abeta) in hippocampus of rats. METHODS: Forty male SPF grade SD rats were divided into four groups: control group (0.9% NaCl), 10 mg/kg AlCl3 group, 20 mg/kg AlCl3 group, and 30 mg/kg AlCl3 group, respectively. After treatment for 8 weeks, the APP methylation level and expressions of APP mRNA was detected by methylation specific PCR and quantitative real time PCR, respectively...
May 2016: Wei Sheng Yan Jiu, Journal of Hygiene Research
Pham Dinh Quoc Huy, Quan Van Vuong, Giovanni La Penna, Peter Faller, Mai Suan Li
The classical force field, which is compatible with the Amber force field 99SB, has been obtained for the interaction of Cu(II) with monomer and dimers of amyloid beta peptides using the coordination where Cu(II) is bound to His6, His13 (or His14) and Asp1 with distorted planar geometry. The newly developed force field and molecular dynamics simulation were employed to study the impact of Cu(II) binding on structures and dynamics of Aβ42 monomer and dimers. It was shown that in the presence of Cu(II) the beta content of monomer is reduced substantially compared to the wild type Aβ42 suggesting that, in accord with experiments, metal ions facilitate formation of amorphous aggregates rather than amyloid fibrils with cross-beta structures...
July 25, 2016: ACS Chemical Neuroscience
Cai-feng Zhu, Jian-jian Sun, Wei Han, Jun Yang
OBJECTIVE: To observe the effect of moxibustion of "Baihui" (GV 20), etc. on learning-memory ability, hip- pocampal amyloid beta (AP) protein expression and immune activity in mild cognitive impairment (MCI) rats, so as to reveal its mechanism underlying improving cognitive impairment. METHODS: A total of 48 SD rats were randomly divided into normal, model, moxibustion, and medication groups (n = 12 in each group). The MCI model was established by intraperitoneal injection of 2 mL mixture solution containing D-galactose (120 mg - kg- - d-) and Sodium Nitrite (90 mg x kg(-1) x d(-1)), once daily for 40 days...
April 2016: Zhen Ci Yan Jiu, Acupuncture Research
Mei-chi Jiang, Jing Liang, Yu-jie Zhang, Jing-rong Wang, Jin-dong Hao, Mei-kang Wang, Jian Xu
OBJECTIVE: To observe the effect of acupuncture stimulation of bilateral "Hegu" (LI 4) and "Taichong" (LR 3, the so-called "Four Gate Points") on learning-memory ability, hippocampal interleukin-1 (IL-1) P and IL-2 and amyloid beta (Abeta) 42 levels in Alzheimer's disease (AD) rats,so as to reveal its underlying mechanism in improving AD. METHODS: Male SD rats were randomly divided into sham operation, model, medication and acupuncture groups (n = 12 rats in each group)...
April 2016: Zhen Ci Yan Jiu, Acupuncture Research
Haruhiko Akiyama
The development of disease-modifying therapy (DMT) that can arrest the pathological processes of Alzheimer's disease (AD) has emerged as one of the highest priorities of medical research. Two pathological hallmarks, amyloid-beta (Abeta) protein deposition and tau accumulation, are the major targets of DMT. Immunotherapy for Abeta removal and secretase inhibitors/modulators that reduce total or accumulation-prone Abeta are candidate DMTs against Abeta. Compounds that prevent tau aggregation are also under development...
April 2016: Brain and Nerve, Shinkei Kenkyū No Shinpo
Wenjing Liu, Heng Cai, Meiqing Lin, Lu Zhu, Lili Gao, Renjia Zhong, Siwei Bi, Yixue Xue, Xiuli Shang
The disruption of blood-brain barrier (BBB) and endothelial cell dysfunction, associated with the cerebrovascular deposition of the amyloid-beta (Abeta) protein, have been characterized as the key pathological characteristics in Alzheimer's disease (AD). In various biologic processes of AD, researchers have proven that mircroRNAs (miRNAs) play critical roles. However, the role and function of miRNAs in the disruption of BBB of AD still remain unclear. Here, we found that mircroRNA-107 (miR-107) is endogenously expressed in human brain microvascular endothelial cells (ECs) of BBB model, while it is significantly down-regulated in ECs pre-incubated with Abeta...
May 1, 2016: Experimental Cell Research
Weigang Cui, Yinghua Zhang, Chenxi Yang, Yiyuan Sun, Min Zhang, Songtao Wang
Neuronal cell apoptosis is an important pathological change in Alzheimer's disease (AD). Hydrogen sulfide (H(2)S) is known to be a novel gaseous signaling molecule and a cytoprotectant in many diseases including AD. However, the molecular mechanism of the antiapoptosis activity of H(2)S in AD is not yet fully understood. The aim of the present study is to evaluate the inhibitory effects of H(2)S on Abeta (Aβ)-induced apoptosis and the molecular mechanisms underlying primary neuron cells. Our results showed that sodium hydrosulfide (NaHS), a donor of H(2)S, significantly ameliorated Aβ-induced cell apoptosis...
June 14, 2016: Neuroscience
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