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Collins-Praino Lyndsey E - - 2014
Alzheimer¿s disease (AD) is the most common neurodegenerative disease and the leading cause of dementia. In addition to grey matter pathology, white matter changes are now recognized as an important pathological feature in the emergence of the disease. Despite growing recognition of the importance of white matter abnormalities in the ...
Lahiri D K DK Indiana UniversitySchool of Medicine, Neuroscience Research Center, 320 West 15th Street, NB 200C, Indianapolis IN 46202, USA. - - 2014
Alzheimer's disease (AD) is characterized by deleterious accumulation of amyloid-β (Aβ) peptide into senile plaque, neurofibrillary tangles formed from hyperphosphorylated tau protein, and loss of cholinergic synapses in the cerebral cortex. The deposition of Aβ-loaded plaques results in microglial activation and subsequent production of reactive oxygen species (ROS), including free ...
Pensalfini Anna A Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, 92697. Electronic address: - - 2014
Genetic analysis of familial forms of Alzheimer's disease (AD) causally links the proteolytic processing of the amyloid precursor protein (APP) and AD. However, the specific type of amyloid and mechanisms of amyloid pathogenesis remain unclear. We conducted a detailed analysis of intracellular amyloid with an aggregation specific conformation dependent monoclonal ...
Holler Christopher J CJ Department of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, KY, USA Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, - - 2014
Recent genome wide association studies have implicated bridging integrator 1 (BIN1) as a late-onset Alzheimer's disease (AD) susceptibility gene. There are at least 15 different known isoforms of BIN1, with many being expressed in the brain including the longest isoform (iso1), which is brain-specific and localizes to axon initial segments ...
Lieury Alice A INSERM U1028, CNRS UMR 5292, Lyon Neuroscience Research Center, Neuro-Oncology and Neuro-Inflammation team, Lyon, France; University Lyon 1, Lyon, - - 2014
Our knowledge of multiple sclerosis (MS) neuropathology has benefited from a number of studies that provided an in-depth description of plaques and, more recently, diffuse alterations of the normal-appearing white or grey matter. However, there have been few studies focusing on the periplaque regions surrounding demyelinated plaques, notably in MS ...
Haider Lukas L Department of Neuroimmunology, Centre for Brain Research, Medical University of Vienna, Vienna, - - 2014
In multiple sclerosis (MS), diffuse degenerative processes in the deep grey matter have been associated with clinical disabilities. We performed a systematic study in MS deep grey matter with a focus on the incidence and topographical distribution of lesions in relation to white matter and cortex in a total sample ...
Maya-Vetencourt José Fernando JF Scuola Normale Superiore, Laboratory of Biology BioSNS, Pisa, - - 2014
Autosomal dominant forms of familial Alzheimer's disease are linked to an aberrant processing of the amyloid-β protein precursor, which results in an increased production of amyloid-β (Aβ) peptides that first form oligomers and eventually aggregate in the form of extracellular amyloid plaques in the brain. The accumulation of Aβ peptides ...
Wu Yili Y Townsend Family Laboratories, Department of Psychiatry, Brain Research Center, Graduate Program in Neuroscience, The University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada, V6T - - 2014
AD, a devastating neurodegenerative disorder, is the most common cause of dementia in the elderly. Patients with AD are characterized by three hallmarks of neuropathology including neuritic plaque deposition, neurofibrillary tangle formation, and neuronal loss. Growing evidences indicate that dysregulation of regulator of calcineurin 1 (RCAN1) plays an important role ...
Hanzel Cecilia E CE Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, - - 2014
Chronic brain inflammation is associated with Alzheimer's disease (AD) and is classically attributed to amyloid plaque deposition. However, whether the amyloid pathology can trigger early inflammatory processes before plaque deposition remains a matter of debate. To address the possibility that a pre-plaque inflammatory process occurs, we investigated the status of ...
Babri Shirin S Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, - - 2014
Alzheimer?s disease (AD) is a neurodegenerative disorder with a progressive cognitive decline and memory loss. Multiple pathogenetic factors including aggregated β-amyloid (Aβ), neurofibrillary tangles (NFTs), cholinergic dysfunction and oxidative stress are involved in AD. Aβ, a major constituent of the senile plaques, is a potent neurotoxic peptide and has a ...
Blair Ja - - 2014
Intraneuronal amyloid-β (iAβ) accumulation has been demonstrated in Alzheimer disease (AD). Although extracellular amyloid plaques composed primarily of aggregated amyloid-β are one of the main pathological features of AD, functional characterization of iAβ is still lacking. In this study, we identified the normal distribution of iAβ through an analysis of ...
Barz Helmut H Holunderweg 17, D-18209 Bad Doberan, Germany. Electronic address: - - 2014
The paper based on the hypothesis that mechanical impulses cause the transmission of excitement in the peripheral and central nervous system. Possible connections between changes in the tubular neuronal network and the morphological findings of Alzheimer's disease are presented. Additionally, changes in the viscosity of the neuronal cytoplasm and changes ...
Ling Daijun - - 2014
Abnormal accumulation of Amyloid beta (Aβ) within autophagy-endosomal- lysosomal (AEL) vesicles is a prominent neuropathological feature of Alzheimer's disease (AD) but the mechanism of accumulation within vesicles is not clear. We express secretory forms of human Aβ1-40 or Aβ1-42 in Drosophila neurons and observe preferential localization of Aβ1-42 within AEL ...
Bloom George S GS Departments of Biology and Cell Biology, University of Virginia, - - 2014
The defining features of Alzheimer disease (AD) include conspicuous changes in both brain histology and behavior. The AD brain is characterized microscopically by the combined presence of 2 classes of abnormal structures, extracellular amyloid plaques and intraneuronal neurofibrillary tangles, both of which comprise highly insoluble, densely packed filaments. The soluble ...
Hamasaki Hideomi H Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, - - 2014
We found that mRNA of MET, the receptor of hepatocyte growth factor (HGF), is significantly decreased in the hippocampus of Alzheimer's disease (AD) patients. Therefore, we tried to determine the cellular component-dependent changes of MET expressions. In this study, we examined cellular distribution of MET in the cerebral neocortices and ...
Pujadas Lluís L 1] Department of Cell Biology, University of Barcelona, Barcelona 08028, Spain [2] Centro de Investigación en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid 28031, Spain [3] Institute for Research in Biomedicine, Barcelona (IRB Barcelona), Barcelona 08028, Spain [4] Vall D'Hebrón Institut de Recerca (VHIR), Barcelona 08035, Spain - - 2014
Reelin is an extracellular matrix protein that is crucial for neural development and adult brain plasticity. While the Reelin signalling cascade has been reported to be associated with Alzheimer's disease (AD), the role of Reelin in this pathology is not understood. Here we use an in vitro approach to show ...
Wang Xiang-Xiang XX Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No. 5 Donghai Middle Road, Qingdao 266071, China ; Department of Neurology, Qingdao Huangdao District People's Hospital, Qingdao 266400, - - 2014
Alzheimer's disease (AD) is the most prevalent type of dementia. Pathological changes in the AD brain include amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs), as well as neuronal death and synaptic loss. Matrix metalloproteinases (MMPs) play an important role as inflammatory components in the pathogenesis of AD. MMP-2 might be ...
Kawakami Ito - - 2014
Tangle-predominant dementia (TPD) is characterized neuropathologically by numerous neurofibrillary tangles in the limbic areas with no or occasional senile plaques throughout the brain. TPD is an under-recognized disease, while it is a common cause of dementia in those over 80 years of age. In the present study, we describe hyperphosphorylated tau ...
van Groen Thomas T Department of Cell, Developmental & Integrative Biology, University of Alabama at Birmingham, 1900 University Boulevard, THT 912, Birmingam, AL 35294-0006, - - 2014
We are studying the projections from the entorhinal cortex to the hippocampal formation in the mouse. The dentate gyrus is innervated by the lateral entorhinal cortex (lateral perforant path) and medial entorhinal cortex (medial perforant path). The entorhinal cortex also projects to hippocampal areas CA3 and CA1, and to the ...
Chen Tong T 0000-0002-7681-9632 School of Biological Sciences, Flinders University, GPO Box 2100, Adelaide, SA 5001, - - 2014
The neuropathological features associated with Alzheimer's disease (AD) include the presence of extracellular amyloid-β peptide-containing plaques and intracellular tau positive neurofibrillary tangles and the loss of synapses and neurons in defined regions of the brain. Dipeptidyl peptidase 10 (DPP10) is a protein that facilitates Kv4 channel surface expression and neuronal ...
Bovier Emily R ER Vision Sciences and Human Biofactors Laboratories, Department of Psychology, The University of Georgia, Athens, Georgia, United States of - - 2014
Lutein and zeaxanthin are major carotenoids in the eye but are also found in post-receptoral visual pathways. It has been hypothesized that these pigments influence the processing of visual signals within and post-retina, and that increasing lutein and zeaxanthin levels within the visual system will lead to increased visual processing ...
Aoki Yasuko Y Department of Neurology, Tokyo Metropolitan Neurological - - 2014
We report an autopsy case of dementia associated with amyotrophic lateral sclerosis (ALS) in a 73-year-old female. She developed memory impairment at the age of 68 years. Atrophy of her hand muscles was noted at the age of 71 years. She was not aware of her memory impairment or muscle ...
Kuchibhotla Kishore V KV Alzheimer's Disease Research Laboratory, Department of Neurology, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA - - 2014
Alzheimer's disease (AD) is pathologically characterized by the deposition of extracellular amyloid-β plaques and intracellular aggregation of tau protein in neurofibrillary tangles (NFTs) (1, 2). Progression of NFT pathology is closely correlated with both increased neurodegeneration and cognitive decline in AD (3) and other tauopathies, such as frontotemporal dementia (4, ...
Li Xiang X Department of Neurology, Changzheng Hospital, Second Military Medical University, Shanghai, - - 2013
Alzheimer's disease (AD) remains a major killer, and although its pathogenesis varies, one dominant feature is an increase in the expression, formation, and sedimentation of senile plaques of amyloid-beta (Aβ) peptides in the brain. The chaperone protein clusterin has, since its fi rst discovery at the end of the 20(th) ...
Liš?i? Rajka M - - 2013
Abstract Alzheimer's dementia (AD) is the most common form of dementia among the elderly, accounting for at least two-thirds of all dementia cases. It represents a costly burden, since its global prevalence is estimated at 24 million cases. Amyloid beta or Aβ plaques and neurofibrillary tangles define AD pathologically but ...
Tan Michelle G - - 2013
Synaptic dysfunction, together with neuritic plaques, neurofibrillary tangles and cholinergic neuron loss is an established finding in the Alzheimer's disease (AD) neocortex. The synaptopathology of AD is known to involve both pre- and postsynaptic components. However, the status of rabphilin 3A (RPH3A), which interacts with the SNARE complex and regulates ...
Tratnjek Larisa - - 2013
Aim. To investigate the involvement of the vesicular membrane trafficking regulator Synaptotagmin IV (Syt IV) in Alzheimer's disease pathogenesis and to define the cell types containing increased levels of Syt IV in the β-amyloid plaque vicinity. Methods. Syt IV protein levels in wild type (WT) and Tg2576 mice cortex were ...
Xie Hong H MassGeneral Institute for Neurodegenerative Diseases, Massachusetts General Hospital, Charlestown, Massachusetts 02129 and School of Life Sciences, Tsinghua University, 100084 Beijing, - - 2013
While accumulation of amyloid-β (Aβ) deposited as senile plaques is a hallmark feature of Alzheimer's disease (AD), the neurotoxicity of these deposits remains controversial. Recent in vitro studies suggested a link between elevated Aβ and mitochondrial dysfunction that might contribute to the pathogenesis of AD. However, the in vivo evidence ...
Andrade-Moraes Carlos Humberto - - 2013
Alzheimer's disease is the commonest cause of dementia in the elderly, but its pathological determinants are still debated. Amyloid-β plaques and neurofibrillary tangles have been implicated either directly as disruptors of neural function, or indirectly by precipitating neuronal death and thus causing a reduction in neuronal number. Alternatively, the initial ...
Gouras Gunnar K - - 2013
Cumulative evidence in brains and cultured neurons of Alzheimer's disease (AD) transgenic mouse models, as well as in human postmortem AD brains, highlights that age-related increases in β-amyloid peptide (Aβ), particularly in endosomes near synapses, are involved in early synapse dysfunction. Our immunoelectron microscopy and high-resolution immunofluorescence microscopy studies show ...
Pooler Amy M - - 2013
Early observations of the patterns of neurofibrillary tangles and amyloid plaques in Alzheimer's disease suggested a hierarchical vulnerability of neurons for tangles, and a widespread nonspecific pattern of plaques that nonetheless seemed to correlate with the terminal zone of tangle bearing neurons in some instances. The first neurofibrillary cortical lesions ...
Kandalepas Patty C PC Department of Cell and Molecular Biology, The Feinberg School of Medicine, Northwestern University, 300 East Superior Street, Tarry 8-713, Chicago, IL 60611-3006, - - 2013
β-Site amyloid precursor protein (APP) cleaving enzyme-1 (BACE1) is the β-secretase that initiates Aβ production in Alzheimer's disease (AD). BACE1 levels are increased in AD, which could contribute to pathogenesis, yet the mechanism of BACE1 elevation is unclear. Furthermore, the normal function of BACE1 is poorly understood. We localized BACE1 ...
Perez-Nievas Beatriz G BG Massachusetts General Hospital ADRC, Harvard University, Boston, MA 02114, - - 2013
Clinico-pathological correlation studies and positron emission tomography amyloid imaging studies have shown that some individuals can tolerate substantial amounts of Alzheimer's pathology in their brains without experiencing dementia. Few details are known about the neuropathological phenotype of these unique cases that might prove relevant to understanding human resilience to Alzheimer's ...
Inaba Tomohiro - - 2013
Biofilms, such as dental plaque, are aggregates of microorganisms attached to a surface. Thus, visualization of the biofilm together with its attached substratum is an important issue in order to understand the detailed interaction between the biofilm and the substratum. However, such techniques are limited. Here, we report a non-invasive ...
Cohen Robert M RM Department of Psychiatry and Behavioral Neurosciences, S Mark Taper Imaging Center, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA. - - 2013
Alzheimer's disease (AD) is hallmarked by amyloid plaques, neurofibrillary tangles, and widespread cortical neuronal loss (Selkoe, 2001). The "amyloid cascade hypothesis" posits that cerebral amyloid sets neurotoxic events into motion that precipitate Alzheimer dementia (Hardy and Allsop, 1991). Yet, faithful recapitulation of all AD features in widely used transgenic (Tg) ...
Howlett David R - - 2013
Genome-wide association studies have pointed to clusterin (apolipoprotein J) as being linked to the occurrence of Alzheimer's disease (AD); studies have identified the protein as a possible biomarker. The association between clusterin and senile plaques in AD brain is well known and clusterin levels in AD brain are 40% higher ...
Uchida Yoko - - 2013
Dystrophic neurites surrounding β-amyloid (Aβ) plaques precede neuronal death in Alzheimer disease. These neuritic alterations may be one of the initial stages for synaptic loss and dysfunction. However, intracellular pathways that cause local disruption of neuronal processes by Aβ remain to be fully elucidated. The identification of Aβ-induced genes that ...
Mitew Stanislaw S Wicking Dementia Research and Education Centre, University of Tasmania Hobart, TAS, Australia ; School of Medicine, University of Tasmania Hobart, TAS, - - 2013
Amyloid-β plaque accumulation in Alzheimer's disease (AD) is associated with dystrophic neurite (DN) formation and synapse loss in principal neurons, but interneuron pathology is less clearly characterized. We compared the responses of neuronal processes immunoreactive for either neurofilament triplet (NF(+)) or calretinin (CR(+)) to fibrillar amyloid (Aβ) plaques in human ...
Raha Animesh Alexander AA John Van Geest Centre for Brain Repair, Department of Clinical Neuroscience, University of Cambridge, Cambridge CB2 0PY, UK. - - 2013
The pathological features of the common neurodegenerative conditions, Alzheimer's disease (AD), Parkinson's disease and multiple sclerosis are all known to be associated with iron dysregulation in regions of the brain where the specific pathology is most highly expressed. Iron accumulates in cortical plaques and neurofibrillary tangles in AD where it ...
Kalimo Hannu H Department of Public Health/Geriatrics, Uppsala University Hospital, Uppsala University, Box 609, SE-751 25, Uppsala, Sweden. - - 2013
The Arctic mutation (p.E693G/p.E22G)fs within the β-amyloid (Aβ) region of the β-amyloid precursor protein gene causes an autosomal dominant disease with clinical picture of typical Alzheimer's disease. Here we report the special character of Arctic AD neuropathology in four deceased patients. Aβ deposition in the brains was wide-spread (Thal phase ...
Hu Kun K Medical Biodynamics Program, Division of Sleep Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, United States. - - 2013
Human motor activity has a robust, intrinsic fractal structure with similar patterns from minutes to hours. The fractal activity patterns appear to be physiologically important because the patterns persist under different environmental conditions but are significantly altered/reduced with aging and Alzheimer's disease (AD). Here, we report that dementia patients, known ...
Sandebring Anna - - 2013
The amyloid-cascade hypothesis posits that the role of amyloid β-peptide (Aβ) in Alzheimer disease (AD) involves polymerization into structures that eventually are deposited as amyloid plaques. During this process, neurotoxic oligomers are formed that induce synaptic loss and neuronal death. Several different isoforms of Aβ are produced, of which the ...
Purushothuman Sivaraman - - 2013
Understanding the response of the brain to haemorrhagic damage is important in haemorrhagic stroke and increasingly in the understanding the cerebral degeneration and dementia that follow head trauma and head-impact sports. In addition, there is growing evidence that haemorrhage from small cerebral vessels is important in the pathogenesis of age-related ...
Iyer Anand - - 2013
Death receptor 6 (DR6) is highly expressed in the human brain: it has been shown to induce axon pruning and neuron death via distinct caspases and to mediate axonal degeneration through binding to N-terminal β amyloid precursor protein (N-APP). We investigated the expression of DR6 during prenatal and postnatal development ...
Trujillo-Estrada Laura L Departamento de Biologia Celular, Genetica y Fisiologia, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, Spain. - - 2013
Alzheimer's disease (AD) is characterized by the abnormal accumulation of extracellular beta-amyloid (Abeta) plaques, intracellular hyperphosphorylated tau, progressive synaptic alterations, axonal dystrophies, neuronal loss and the deterioration of cognitive capabilities of patients. However, no effective disease-modifying treatment has been yet developed. In this work we have evaluated whether chronic lithium ...
Shukla Varsha - - 2012
Alzheimer's disease (AD), the most devastating chronic neurodegenerative disease in adults, causes dementia and eventually, death of the affected individuals. Clinically, AD is characterized as late-onset, age-dependent cognitive decline due to loss of neurons in cortex and hippocampus. The pathologic corollary of these symptoms is the formation of senile plaques ...
Li Jian-Ming - - 2012
The spinal cord is composed of distinct neuronal groups with well-defined anatomic connections. In some transgenic (Tg) models of Alzheimer's disease (AD), amyloid plaques develop in this structure, although the underlying cellular mechanism remains elusive. We attempted to explore the origin, evolution, and modulation of spinal β-amyloid (Aβ) deposition using ...
Rudinskiy Nikita - - 2012
Experience-induced expression of immediate-early gene Arc (also known as Arg3.1) is known to be important for consolidation of memory. Using in vivo longitudinal multiphoton imaging, we found orchestrated activity-dependent expression of Arc in the mouse extrastriate visual cortex in response to a structured visual stimulation. In wild-type mice, the amplitude ...
Darvesh Sultan - - 2012
Butyrylcholinesterase (BuChE) is found to have a brain distribution pattern that is distinct from that of acetylcholinesterase (AChE). Neurons containing BuChE are particularly located in the amygdala, hippocampal formation and the thalamus, structures involved in the normal functions of cognition and behavior that typically become compromised in Alzheimer's disease (AD). ...
Honea Robyn A RA Department of Neurology, University of Kansas School of Medicine, Kansas City, - - 2012
Despite behavioral differences between genetic subtypes of Prader-Willi syndrome (PWS), no studies have been published characterizing brain structure in these subgroups. Our goal was to examine differences in the brain structure phenotype of common subtypes of PWS [chromosome 15q deletions and maternal uniparental disomy 15 (UPD)]. Fifteen individuals with PWS ...
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