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https://www.readbyqxmd.com/read/28719018/ante-mortem-csf-tau-levels-correlate-with-post-mortem-tau-pathology-in-ftld
#1
D J Irwin, A Lleó, S X Xie, C T McMillan, D Wolk, E B Lee, V M Van Deerlin, L M Shaw, J Q Trojanowski, M Grossman
OBJECTIVE: To test the hypotheses that 1) antemortem cerebrospinal fluid tau levels correlate with postmortem tau pathology in frontotemporal lobar degeneration and 2) tauopathy patients have higher phosphorylated-tau levels compared to TDP-43 proteinopathy patients while accounting for Alzheimer's disease co-pathology. METHODS: Patients had autopsy-confirmed frontotemporal lobar degeneration with tauopathy (n=31), TDP-43 proteinopathy (n=49), or Alzheimer's disease (n=26) with antemortem cerebrospinal fluid...
July 18, 2017: Annals of Neurology
https://www.readbyqxmd.com/read/28716886/clinical-neurology-and-epidemiology-of-the-major-neurodegenerative-diseases
#2
Michael G Erkkinen, Mee-Ohk Kim, Michael D Geschwind
Neurodegenerative diseases are a common cause of morbidity and cognitive impairment in older adults. Most clinicians who care for the elderly are not trained to diagnose these conditions, perhaps other than typical Alzheimer's disease (AD). Each of these disorders has varied epidemiology, clinical symptomatology, laboratory and neuroimaging features, neuropathology, and management. Thus, it is important that clinicians be able to differentiate and diagnose these conditions accurately. This review summarizes and highlights clinical aspects of several of the most commonly encountered neurodegenerative diseases, including AD, frontotemporal dementia (FTD) and its variants, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), Parkinson's disease (PD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), and Huntington's disease (HD)...
July 17, 2017: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/28716398/serotonin-depletion-increases-seizure-susceptibility-and-worsens-neuropathological-outcomes-in-kainate-model-of-epilepsy
#3
Gisela H Maia, Cátia S Brazete, Joana I Soares, Liliana L Luz, Nikolai V Lukoyanov
Serotonin is implicated in the regulation of seizures, but whether or not it can potentiate the effects of epileptogenic factors is not fully established. Using the kainic acid model of epilepsy in rats, we tested the effects of serotonin depletion on (1) susceptibility to acute seizures, (2) development of spontaneous recurrent seizures and (3) behavioral and neuroanatomical sequelae of kainic acid treatment. Serotonin was depleted by pretreating rats with p-chlorophenylalanine. In different groups, kainic acid was injected at 3 different doses: 6...
July 14, 2017: Brain Research Bulletin
https://www.readbyqxmd.com/read/28715661/cognitive-decline-and-brain-amyloid-%C3%AE-accumulation-across-3-years-in-adults-with-down-syndrome
#4
Sigan L Hartley, Benjamin L Handen, Darlynne Devenny, Iulia Mihaila, Regina Hardison, Patrick J Lao, William E Klunk, Peter Bulova, Sterling C Johnson, Bradley T Christian
Adults with Down syndrome (DS) have a high incidence of Alzheimer's disease (AD), providing a unique opportunity to explore the early, preclinical stages of AD neuropathology. We examined change in brain amyloid-β accumulation via the positron emission tomography tracer [11C] Pittsburgh compound B (PiB) across 2 data collection cycles, spaced 3 years apart, and decline in cognitive functioning in 58 adults with DS without clinical AD. PiB retention increased in the anterior cingulate gyrus, precuneus cortex, parietal cortex, and anterior ventral striatum...
June 2, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28715425/elimination-of-huntingtin-in-the-adult-mouse-leads-to-progressive-behavioral-deficits-bilateral-thalamic-calcification-and-altered-brain-iron-homeostasis
#5
Paula Dietrich, Irudayam Maria Johnson, Shanta Alli, Ioannis Dragatsis
Huntington's Disease (HD) is an autosomal dominant progressive neurodegenerative disorder characterized by cognitive, behavioral and motor dysfunctions. HD is caused by a CAG repeat expansion in exon 1 of the HD gene that is translated into an expanded polyglutamine tract in the encoded protein, huntingtin (HTT). While the most significant neuropathology of HD occurs in the striatum, other brain regions are also affected and play an important role in HD pathology. To date there is no cure for HD, and recently strategies aiming at silencing HTT expression have been initiated as possible therapeutics for HD...
July 17, 2017: PLoS Genetics
https://www.readbyqxmd.com/read/28715400/a-novel-method-to-model-chronic-traumatic-encephalopathy-in-drosophila
#6
Mingkuan Sun, Liam L Chen
Chronic Traumatic Encephalopathy (CTE) is an established neurodegenerative disease that is closely associated with exposure to repetitive mild Traumatic Brain Injury (mTBI). The mechanisms responsible for its complex pathological changes remain largely elusive, despite a recent consensus to define the neuropathological criteria. Here, we describe a novel method to develop a model of CTE in Drosophila melanogaster (Drosophila ) in an attempt to identify the key genes and pathways that lead to the characteristic hyperphosphorylated tau accumulation and neuronal death in the brain...
July 4, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/28714776/tissue-localization-of-glycosphingolipid-accumulation-in-a-gaucher-disease-mouse-brain-by-lc-esi-ms-ms-and-high-resolution-maldi-imaging-mass-spectrometry
#7
E Ellen Jones, Wujuan Zhang, Xueheng Zhao, Cristine Quiason, Stephanie Dale, Sheerin Shahidi-Latham, Gregory A Grabowski, Kenneth D R Setchell, Richard R Drake, Ying Sun
To better understand regional brain glycosphingolipid (GSL) accumulation in Gaucher disease (GD) and its relationship to neuropathology, a feasibility study using mass spectrometry and immunohistochemistry was conducted using brains derived from a GD mouse model (4L/PS/NA) homozygous for a mutant GCase (V394L [4L]) and expressing a prosaposin hypomorphic (PS-NA) transgene. Whole brains from GD and control animals were collected using one hemisphere for MALDI FTICR IMS analysis and the other for quantitation by LC-ESI-MS/MS...
July 1, 2017: SLAS Discovery
https://www.readbyqxmd.com/read/28711290/biopsies-of-pediatric-brainstem-lesions-display-low-morbidity-but-strong-impact-on-further-treatment-decisions
#8
Johanna Quick-Weller, Stephanie Tritt, Bedjan Behmanesh, Michel Mittelbronn, Andrea Spyrantis, Nazife Dinc, Lutz Weise, Volker Seifert, Gerhard Marquardt, Thomas M Freiman
OBJECTIVE: The course of malignant brain stem gliomas in childhood is rarely positive. Because of limited therapeutic options and potentially hazardous biopsies oncologist often relay on MRI diagnoses only for further therapy decisions. In this study we show that brain stem biopsies display a low morbidity rate and neuropathological assessment has a considerable impact on further treatment decision. METHODS: Within 18-months five children with brainstem symptoms and the radiological diagnosis of a malignant brainstem glioma, were identified...
July 12, 2017: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
https://www.readbyqxmd.com/read/28710387/protein-tyrosine-phosphatase-inhibition-prevents-experimental-cerebral-malaria-by-precluding-cxcr3-expression-on-t-cells
#9
Kristin M Van Den Ham, Logan K Smith, Martin J Richer, Martin Olivier
Cerebral malaria induced by Plasmodium berghei ANKA infection is dependent on the sequestration of cytotoxic T cells within the brain and augmentation of the inflammatory response. Herein, we demonstrate that inhibition of protein tyrosine phosphatase (PTP) activity significantly attenuates T cell sequestration within the brain and prevents the development of neuropathology. Mechanistically, the initial upregulation of CXCR3 on splenic T cells upon T cell receptor stimulation was critically decreased through the reduction of T cell-intrinsic PTP activity...
July 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28708131/a-clinicopathological-approach-to-the-diagnosis-of-dementia
#10
REVIEW
Fanny M Elahi, Bruce L Miller
The most definitive classification systems for dementia are based on the underlying pathology which, in turn, is categorized largely according to the observed accumulation of abnormal protein aggregates in neurons and glia. These aggregates perturb molecular processes, cellular functions and, ultimately, cell survival, with ensuing disruption of large-scale neural networks subserving cognitive, behavioural and sensorimotor functions. The functional domains affected and the evolution of deficits in these domains over time serve as footprints that the clinician can trace back with various levels of certainty to the underlying neuropathology...
July 14, 2017: Nature Reviews. Neurology
https://www.readbyqxmd.com/read/28708110/cognitive-changes-in-the-spinocerebellar-ataxias-due-to-expanded-polyglutamine-tracts-a-survey-of-the-literature
#11
REVIEW
Evelyn Lindsay, Elsdon Storey
The dominantly-inherited ataxias characterised by expanded polyglutamine tracts-spinocere bellar ataxias (SCAs) 1, 2, 3, 6, 7, 17, dentatorubral pallidoluysian atrophy (DRPLA) and, in part, SCA 8-have all been shown to result in various degrees of cognitive impairment. We survey the literature on the cognitive consequences of each disorder, attempting correlation with their published neuropathological, magnetic resonance imaging (MRI) and clinical features. We suggest several psychometric instruments for assessment of executive function, whose results are unlikely to be confounded by visual, articulatory or upper limb motor difficulties...
July 14, 2017: Brain Sciences
https://www.readbyqxmd.com/read/28708055/prion-disease-pathogenesis-in-the-absence-of-the-commensal-microbiota
#12
Barry M Bradford, Laura Tetlow, Neil A Mabbott
Prion diseases are a unique group of transmissible, typically sub-acute, neurodegenerative disorders. During central nervous system (CNS) prion disease, the microglia become activated and are thought to provide a protective response by scavenging and clearing prions. The mammalian intestine is host to a large burden of commensal micro-organisms, especially bacteria, termed the microbiota. The commensal microbiota has beneficial effects on host health, including through the metabolism of essential nutrients, regulation of host development and protection against pathogens...
July 15, 2017: Journal of General Virology
https://www.readbyqxmd.com/read/28707805/decreased-parvalbumin-mrna-levels-in-cerebellar-purkinje-cells-in-autism
#13
Jean-Jacques Soghomonian, Kunzhong Zhang, Sujithra Reprakash, Gene J Blatt
Recent neuropathology studies in human brains indicate that several areas of the prefrontal cortex have decreased numbers of parvalbumin interneurons or decreased parvalbumin expression in Autism Spectrum disorders (ASD) [Hashemi, Ariza, Rogers, Noctor, & Martinez-Cerdeno, 2017; Zikopoulos & Barbas, ]. These data suggest that a deficit in parvalbumin may be a key neuropathology of ASD and contribute to altered GABAergic inhibition. However, it is unclear if a deficit in parvalbumin is a phenomenon that occurs in regions other than the cerebral cortex...
July 14, 2017: Autism Research: Official Journal of the International Society for Autism Research
https://www.readbyqxmd.com/read/28707717/an-autopsied-case-of-corticobasal-degeneration-presenting-with-frontotemporal-dementia-followed-by-myoclonus
#14
Yasushi Iwasaki, Keiko Mori, Masumi Ito, Maya Mimuro, Mari Yoshida
A Japanese woman developed frontotemporal dementia (FTD)-like symptoms of abnormal behavior, such as stereotyped behavior and disinhibition. The patient developed these symptoms at the age of 59 years, although aphasia symptoms were not apparent at early disease stages. Progressive parkinsonism was dominant on the left side, and conspicuous myoclonus was recognized in the late disease stage. MRI indicated severe, right side-dominant frontotemporal lobe atrophy with white matter degeneration. Brainstem and cerebellar atrophy were also observed...
July 14, 2017: Neuropathology: Official Journal of the Japanese Society of Neuropathology
https://www.readbyqxmd.com/read/28707657/-transmission-of-pathogenic-protein-aggregates-in-alzheimer-s-disease
#15
A L Schwarzman, S V Sarantseva
Deposits of amyloid peptide Aβ and intracellular aggregates of hyperphosphorylated tau protein in the brain of patients are major neuropathological features of Alzheimer's disease (AD). For a long time, the possibility of horizontal transmission of Aβ aggregates from cell to cell and from person to person remained hypothetical, since there was no experimental evidence. However, in 1993, the formation of senile plaques was confirmed in the brains of animals after intracerebral injections of AD patient brain homogenates or homogenates of the brain of transgenic mice enriched with Aβ aggregates...
May 2017: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/28705658/disturbance-of-redox-homeostasis-in-down-syndrome-role-of-iron-dysmetabolism
#16
REVIEW
Eugenio Barone, Andrea Arena, Elizabeth Head, D Allan Butterfield, Marzia Perluigi
Down syndrome (DS) is the most common genetic form of intellectual disability that leads in the majority of cases to development of early-onset Alzheimer-like dementia (AD). The neuropathology of DS has several common features with AD including alteration of redox homeostasis, mitochondrial deficits, and inflammation among others. Interestingly, some of the genes encoded by chromosome 21 are responsible of increased oxidative stress (OS) conditions that are further exacerbated by decreased antioxidant defense...
July 10, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28704930/mitochondrial-dysfunction-mediated-by-poly-adp-ribose-polymerase-1-activation-contributes-to-hippocampal-neuronal-damage-following-status-epilepticus
#17
Yi-Chen Lai, J Scott Baker, Taraka Donti, Brett H Graham, William J Craigen, Anne E Anderson
Mitochondrial dysfunction plays a central role in the neuropathology associated with status epilepticus (SE) and is implicated in the development of epilepsy. While excitotoxic mechanisms are well-known mediators affecting mitochondrial health following SE, whether hyperactivation of poly(ADP-ribose) polymerase-1 (PARP-1) also contributes to SE-induced mitochondrial dysfunction remains to be examined. Here we first evaluated the temporal evolution of poly-ADP-ribosylated protein levels in hippocampus following kainic acid-induced SE as a marker for PARP-1 activity, and found that PARP-1 was hyperactive at 24 h following SE...
July 12, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28704198/alzheimer-s-disease-as-it-was-in-the-beginning
#18
REVIEW
Stanislav Kozlov, Alexei Afonin, Igor Evsyukov, Andrei Bondarenko
Since Alzheimer's disease was first described in 1907, many attempts have been made to reveal its main cause. Nowadays, two forms of the disease are known, and while the hereditary form of the disease is clearly caused by mutations in one of several genes, the etiology of the sporadic form remains a mystery. Both forms share similar sets of neuropathological and molecular manifestations, including extracellular deposition of amyloid-beta, intracellular accumulation of hyperphosphorylated tau protein, disturbances in both the structure and functions of mitochondria, oxidative stress, metal ion metabolism disorders, impairment of N-methyl-D-aspartate receptor-related signaling pathways, abnormalities of lipid metabolism, and aberrant cell cycle reentry in some neurons...
July 12, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28703027/life-course-determinants-of-cognitive-reserve-cr-in-cognitive-aging-and-dementia-a-systematic-literature-review
#19
Dorota Chapko, Roisin McCormack, Corri Black, Roger Staff, Alison Murray
OBJECTIVES: The concept of cognitive reserve (CR) is defined as a moderator, which allows an individual to preserve cognition despite underlying brain pathology. There is no consensus of what potentially modifiable CR determinants are of greatest importance. The aim of this review was to identify life-course factors which protect older individuals from expressing cognitive decline despite the presence of brain pathology. METHOD: A systematic review search was performed in MEDLINE (1946-06/09/13), EMBASE (1947-06/09/13), and PsycheInfo (1967-06/09/13)...
July 13, 2017: Aging & Mental Health
https://www.readbyqxmd.com/read/28699522/targeting-human-astrocytes-calcium-sensing-receptors-for-treatment-of-alzheimer-s-disease
#20
Anna Chiarini, Ubaldo Armato, James F Whitfield, Ilaria Dal Pra
Understanding the pathophysiology of Alzheimer's disease (AD) in the principal human neural cells is necessary for finding therapeutics for this illness. To help do this, we have been using freshly cultured functionally normal cerebral cortical adult human astrocytes (NAHAs) and postnatal neurons. The findings show that amyloid-β oligomers (Aβ-os) binding to calcium-sensing receptors (CaSRs) on NAHAs and neuron surfaces trigger signals capable of driving AD pathogenesis. This Aβ•CaSR signalling shifts the amyloid precursor protein (APP) from its α-secretase shedding producing neurotrophic/neuroprotective soluble (s)APPα to its β-secretase cleaving engendering AD-driving Aβ42/Aβ42-os peptides...
July 10, 2017: Current Pharmaceutical Design
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