95 results match your criteria American journal of neurodegenerative disease[Journal]


Translational inhibition of α-synuclein by Posiphen normalizes distal colon motility in transgenic Parkinson mice.

Am J Neurodegener Dis 2019 15;8(1):1-15. Epub 2019 Feb 15.

QR Pharma 1055 Westlakes Drive, Berwyn PA 19312, USA.

Parkinson disease (PD) is a neurodegenerative disease with motor as well as non-motor symptoms, including gastrointestinal dysfunction. In humans, these precede the motor symptoms by decades. Previously developed and characterized transgenic mice expressing the mutant human α-synuclein gene () (either A53T or A30P), but not the endogenous mouse , serve as models for familial PD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6420700PMC
February 2019
1 Read

Overexpression of , , improves motor neuron degeneration induced by knockdown of , .

Am J Neurodegener Dis 2018 5;7(1):11-31. Epub 2018 Feb 5.

Department of Applied Biology, Kyoto Institute of TechnologyMatsugasaki, Sakyo-ku, Kyoto, Japan.

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive neurodegenerative disease characterized by the motor neuron degeneration that eventually leads to complete paralysis and death within 2-5 years after disease onset. One of the major pathological hallmark of ALS is abnormal accumulation of inclusions containing TAR DNA-binding protein-43 (TDP-43). TDP-43 is normally found in the nucleus, but in ALS, it localizes in the cytoplasm as inclusions as well as in the nucleus. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840287PMC
February 2018
4 Reads

The protective effects of crocin in the management of neurodegenerative diseases: a review.

Am J Neurodegener Dis 2018 5;7(1):1-10. Epub 2018 Feb 5.

Department of Neurosurgery, Faculty of Medicine, Mashhad University of Medical SciencesMashhad, Iran.

Flavonoids have been used in traditional medicine to promote human health. Crocin has been proposed to be effective in the management of the various diseases including the neurodegenerative diseases. Antiepileptic and anti-Alzheimer effects of crocin have also been indicated. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840286PMC
February 2018
6 Reads

One case with dexmedetomidine-induced stuporous state in epileptic patient undergoing abdominal surgery.

Am J Neurodegener Dis 2017 25;6(3):26-31. Epub 2017 Jul 25.

Department of Anesthesiology and Pain Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and TechnologyWuhan 430030, Hubei, China.

A 56-year-old epileptic patient underwent right hemicolectomy and cholecystectomy surgery under general endotracheal anesthesia. Anesthesia was maintained with sevoflurane, and sufentanil, rocuronium, and dexmedetomidine infusions. After the operation and confirmation of neuromuscular recovery, the patient woke from anesthesia within 15 min and successfully extubated. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5545215PMC
July 2017
7 Reads

Altered mechanisms of protein synthesis in frontal cortex in Alzheimer disease and a mouse model.

Am J Neurodegener Dis 2017 15;6(2):15-25. Epub 2017 Jun 15.

Institute of Neuropathology, Pathologic Anatomy Service, Bellvitge University HospitalIDIBELL, Spain.

Expression of the nucleolar chaperones nucleolin () and nucleophosmin (), upstream binding transcription factor (), rRNA18S, rRNA28S, and several genes encoding ribosomal proteins (RPs) is decreased in frontal cortex area 8 at advanced stages of Alzheimer's disease (AD). This is accompanied by reduced protein levels of elongation factors eEF1A and eEF2. Changes are more marked in AD cases with rapid course (rpAD), as initiation factor eIF3η is significantly down-regulated and several RP genes up-regulated in rpAD when compared with typical AD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498849PMC
June 2017
21 Reads

Can levodopa prevent cognitive decline in patients with Parkinson's disease?

Am J Neurodegener Dis 2017 15;6(2):9-14. Epub 2017 Jun 15.

Department of Neurology, Nara Medical UniversityKashihara, Nara, Japan.

Cognitive impairment in Parkinson's disease (PD) will become more important since the number of elderly patients with PD is increasing. We prospectively studied non-demented patients with PD over the course of 3 years to identify factors associated with PD that contribute to a decline in cognitive function. From among 100 consecutive patients, we registered 79 patients with PD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5498848PMC
June 2017
25 Reads

Etiology and treatment of amyotrophic lateral sclerosis.

Am J Neurodegener Dis 2017 15;6(1):1-8. Epub 2017 Apr 15.

General Surgeon, Clínica Santa MónicaLima, Peru.

Background: To date all researchers conclude that the etiology of Amyotrophic lateral sclerosis (ALS) is not known. On the contrary, since August 2009, we believe that disease is of ischemic origin in the anterior surface of the medulla oblongata.

Material And Method: We present our surgical experience into 45 patients with ALS (bulbar form in 36 cases and spinal form in 9). Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5435608PMC
April 2017
21 Reads

Metabolic, inflammatory, and microvascular determinants of white matter disease and cognitive decline.

Am J Neurodegener Dis 2016 30;5(5):171-177. Epub 2016 Nov 30.

Department of Internal Medicine, Division of Cardiology, University of California Davis USA.

White Matter Disease is increasingly being recognized as an important cause of cognitive decline and dementia. Various investigations have linked chronic diet-related conditions to the development of white matter lesions, which appear as white matter hyperintensities on T2-weighted magnetic resonance imaging (MRI) scans of the brain. Thus, it can be postulated that the metabolic, inflammatory, and microvascular changes accompanying a western diet, hyperlipidemia, hypertension, and diabetes mellitus type II (DMII) are potential mediators in the development and progression of white matter disease, which in turn contributes to the development and progression of cognitive decline. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5218857PMC
November 2016
3 Reads

Chemical and neuropathological analyses of an Alzheimer's disease patient treated with solanezumab.

Am J Neurodegener Dis 2016 26;5(4):158-170. Epub 2016 Aug 26.

Laboratory of Neuropathology, Banner Sun Health Research Institute Sun City, AZ 85351.

Introduction: Based on the amyloid cascade hypothesis of Alzheimer's disease (AD) pathogenesis, a series of clinical trials involving immunotherapies have been undertaken including infusion with the IgG1 monoclonal anti-Aβ antibody solanezumab directed against the middle of the soluble Aβ peptide. In this report, we give an account of the clinical history, psychometric testing, gross and microscopic neuropathology as well as immunochemical quantitation of soluble and insoluble Aβ peptides and other proteins of interest related to AD pathophysiology in a patient treated with solanezumab.

Materials And Methods: The solanezumab-treated AD case (SOLA-AD) was compared to non-demented control (NDC, n = 5) and non-immunized AD (NI-AD, n = 5) subjects. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5043095PMC
August 2016
4 Reads

Omental transplantation in a patient with mild ALS.

Authors:
Hernando Rafael

Am J Neurodegener Dis 2016 6;5(3):153-7. Epub 2016 Jul 6.

Neurosurgeon, Clínica Santa Mónica Lima, Perú

To demonstrate that amyotrophic lateral sclerosis (ALS) is not a neurodegenerative disease. The patient, a 33-year-old man began with symptoms of the bulbar form of ALS, characterized by burning pain in both feet during two months and then, he presented right crural monoparesis, fasciculations, slight dysarthria and he walked with help of orthopedic devices. A preoperative MRI scans showed atherosclerosis at the V4 segment of the left vertebral artery. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4965616PMC

Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease [Retraction].

Authors:

Am J Neurodegener Dis 2016 6;5(3):152. Epub 2016 Jul 6.

[This retracts the article on p. 1 in vol. 5, PMID: 27073740. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4965615PMC

Effect of fish oil on glutathione redox system in multiple sclerosis.

Am J Neurodegener Dis 2016 1;5(2):145-51. Epub 2016 Jun 1.

OPD Instituto Jalisciense de Cancerología SSA-Jalisco. Guadalajara, Jalisco. México.

Unlabelled: Multiple sclerosis (MS) is a chronic, inflammatory and autoimmune disease of the central nervous system. Dysregulation of glutathione homeostasis and alterations in glutathione-dependent enzyme activities are implicated in the induction and progression of MS. Evidence suggests that Omega-3 polyunsaturated fatty acids (PUFAs) have anti-inflammatory, antioxidant and neuroprotective effects. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913222PMC
June 2016
3 Reads

Ganoderma Lucidum polysaccharides protect against MPP(+) and rotenone-induced apoptosis in primary dopaminergic cell cultures through inhibiting oxidative stress.

Am J Neurodegener Dis 2016 1;5(2):131-44. Epub 2016 Jun 1.

Institute for Medical Biochemistry, University for Veterinary Medicine Veterinaerplatz 1, A-1210 Vienna, Austria.

Oxidative stress plays a pivotal role in the progressive neurodegeneration in Parkinson's disease (PD) which is responsible for disabling motor abnormalities in more than 6.5 million people worldwide. Polysaccharides are the main active constituents from Ganoderma lucidum which is characterized with anti-oxidant, antitumor and immunostimulant properties. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913221PMC
June 2016
4 Reads

Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease in focal cerebral ischemic rats.

Am J Neurodegener Dis 2016 1;5(2):102-30. Epub 2016 Jun 1.

Sleep Disorders Group, EEE/Melbourne School of Engineering, The University of Melbourne Parkville, Victoria 3010, Australia.

Alzheimer's disease (AD) is a chronic progressive neurodegenerative condition of the brain, and it is the most common cause of dementia. Several neurobiological etiologies of AD are described in the literature. These include vascular, infectious, toxic, nutritional, metabolic, and inflammatory. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4913220PMC
June 2016
1 Read
7 Citations

The presenilin 1 p.Gly206Ala mutation is a frequent cause of early-onset Alzheimer's disease in Hispanics in Florida.

Am J Neurodegener Dis 2016 1;5(1):94-101. Epub 2016 Mar 1.

Department of Neuroscience, Mayo Clinic Jacksonville, FL, 32224 USA.

Mutations in the gene encoding the presenilin-1 protein (PSEN1) were first discovered to cause Alzheimer's disease (AD) 20 years ago. Since then more than 200 different pathogenic mutations have been reported, including a p.Gly206Ala founder mutation in the Hispanic population. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788736PMC
April 2016
25 Reads

Association study between the DNMT3A -448A>G polymorphism and risk of Alzheimer's disease in Caucasians of Italian origin.

Am J Neurodegener Dis 2016 1;5(1):85-93. Epub 2016 Mar 1.

Department of Translational Research and New Technologies in Medicine and Surgery, Section of Medical Genetics, University of PisaVia Roma 55, 56126 Pisa, Italy; Interdepartmental Research Center Nutrafood "Nutraceuticals and Food for Health", University of PisaVia del Borghetto 80, 56124 Pisa, Italy.

Increasing evidence points to an epigenetic contribution in Alzheimer's disease (AD) pathogenesis. In this regard, variants and polymorphisms of DNA methyltransferase genes (DNMTs) are being investigated for their contribution to cognitive decline and dementia, but results are still scarce or controversial. In the present study we genotyped 710 Caucasian subjects of Italian descent, including 320 late-onset AD (LOAD) patients, 70 individuals with amnestic Mild Cognitive Impairment (MCI), and 320 matched healthy controls, for the presence of a functional DNMT3A -448A>G (rs1550117) polymorphism, searching for association with disease risk. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788735PMC
April 2016
21 Reads

Molecular events linking cholesterol to Alzheimer's disease and inclusion body myositis in a rabbit model.

Am J Neurodegener Dis 2016 1;5(1):74-84. Epub 2016 Mar 1.

Department of Basic Sciences, School of Medicine and Health Sciences, University of North Dakota Grand Forks, ND 58202, USA.

Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by cognitive impairment and dementia, resulting from progressive synaptic dysfunction, loss and neuronal cell death. Inclusion body myositis (IBM) is a skeletal muscle degenerative disease, displaying progressive proximal and distal muscle weakness, in association with muscle fiber atrophy, degeneration and death. Studies have shown that the late onset version of AD (LOAD) and sporadic IBM (sIBM) in muscle share many pathological features, including the presence of extracellular plaques of β-amyloid peptides and intracellular tangles of hyperphosphorylated tau proteins. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788734PMC
April 2016
13 Reads

Pyruvate blocks blood-brain barrier disruption, lymphocyte infiltration and immune response in excitotoxic brain injury.

Am J Neurodegener Dis 2016 1;5(1):69-73. Epub 2016 Mar 1.

Department of Anesthesiology, Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia Vancouver, BC, V6T 1Z3, Canada.

The effects of pyruvate, the end metabolite of glycolysis, on blood-brain barrier (BBB) impairment and immune reactivity were examined in the quinolinic acid (QA)-injected rat striatum. Extensive disruption of BBB was observed at 7 d post QA-injection as demonstrated by increased immunohistochemical staining using antibody against immunoglobulin G (IgG). Animals receiving pyruvate administration (500 mg/kg) with QA-injection exhibited reduced lgG immunoreactivity (by 45%) relative to QA alone. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788733PMC
April 2016
1 Read

Ebi, a Drosophila homologue of TBL1, regulates the balance between cellular defense responses and neuronal survival.

Am J Neurodegener Dis 2016 1;5(1):62-8. Epub 2016 Mar 1.

Center for Development of Advanced Medicine for Dementia (CAMD), National Center for Geriatrics and Gerontology (NCGG), Obu Aichi, Japan.

Transducin β-like 1 (TBL1), a transcriptional co-repressor complex, is a causative factor for late-onset hearing impairments. Transcriptional co-repressor complexes play pivotal roles in gene expression by making a complex with divergent transcription factors. However, it remained to be clarified how co-repressor complex regulates cellular survival. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788732PMC
April 2016
4 Reads

Ginsenoside Rd and ginsenoside Re offer neuroprotection in a novel model of Parkinson's disease.

Am J Neurodegener Dis 2016 1;5(1):52-61. Epub 2016 Mar 1.

Institute of Chemistry and Biochemistry, Veterinary Medical University Vienna Veterinaerplatz 1, A-1210 Vienna, Austria.

Ginsenosides are the main active constituents of Panax ginseng. Ginsenoside Re is one of the major ginsenosides; whereas hydrolysis products such as Rd appear to have higher biological activity though are present in smaller amounts. Ginsenosides, from their early use in folk medicine to modern studies, appear to exert beneficial actions against aging and even neurodegenerative disorders. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788731PMC
April 2016
4 Reads

Repurposing psychiatric medicines to target activated microglia in anxious mild cognitive impairment and early Parkinson's disease.

Am J Neurodegener Dis 2016 1;5(1):29-51. Epub 2016 Mar 1.

Department of Psychiatry and Behavioral Sciences, Mercer University School of Medicine 655 First Street, Macon, Georgia, 31201, USA.

Anxiety is common in the Mild Cognitive Impairment (MCI) stage of Alzheimer's disease (AD) and the pre-motor stages of Parkinson's disease (PD). A concomitant and possible cause of this anxiety is microglial activation, also considered a key promoter of neurodegeneration in MCI and early PD via inflammatory mechanisms and the generation of degenerative proinflammatory cytokines. Psychiatric disorders, prevalent in AD and PD, are often treated with psychiatric drugs (psychotropics), raising the question of whether psychotropics might therapeutically affect microglial activation, MCI, and PD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788730PMC
April 2016
8 Reads

Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease.

Am J Neurodegener Dis 2016 1;5(1):1-28. Epub 2016 Mar 1.

Sleep Disorders Group, EEE/Melbourne School of Engineering, The University of Melbourne Parkville, Victoria 3010, Australia.

Alzheimer's disease (AD) is a chronic progressive neurodegenerative condition of the brain, and it is the most common cause of dementia. Several neurobiological etiologies of AD are described in the literature. These include vascular, infectious, toxic, nutritional, metabolic, and inflammatory. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4788729PMC
April 2016
4 Citations

Erratum: Development, appraisal, validation and implementation of a consensus protocol for the assessment of cerebral amyloid angiopathy in post-mortem brain tissue.

Am J Neurodegener Dis 2015 28;4(2):49. Epub 2015 Dec 28.

Dementia Research Group, School of Clinical Sciences, University of Bristol UK.

In a collaboration involving 11 groups with research interests in cerebral amyloid angiopathy (CAA), we used a two-stage process to develop and in turn validate a new consensus protocol and scoring scheme for the assessment of CAA and associated vasculopathic abnormalities in post-mortem brain tissue. Stage one used an iterative Delphi-style survey to develop the consensus protocol. The resultant scoring scheme was tested on a series of digital images and paraffin sections that were circulated blind to a number of scorers. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700126PMC
January 2016
24 Reads

Transcription factor Sp1 inhibition, memory, and cytokines in a mouse model of Alzheimer's disease.

Am J Neurodegener Dis 2015 28;4(2):40-8. Epub 2015 Dec 28.

Department of Cellular and Molecular Biology, USFTampa, FL 33620; Current Address: NeuroEM Therapeutics, Inc.Phoenix, AZ 85022.

Transcription factors are involved to varying extents in the health and survival of neurons in the brain and a better understanding of their roles with respect to the pathogenesis of Alzheimer's disease (AD) could lead to the development of additional treatment strategies. Sp1 is a transcription factor that responds to inflammatory signals occurring in the AD brain. It is known to regulate genes with demonstrated importance in AD, and we have previously found it upregulated in the AD brain and in brains of transgenic AD model mice. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700125PMC
January 2016
11 Reads

Anti-inflammatory therapies of amyotrophic lateral sclerosis guided by immune pathways.

Am J Neurodegener Dis 2015 28;4(2):28-39. Epub 2015 Dec 28.

Department of Surgery, UCLA School of Medicine Los Angeles, CA 90095-7022.

Sporadic ALS patients display heterogeneous immune pathways in peripheral blood mononuclear cells (PBMCs). We tested nine sALS patients and one unaffected identical twin of an index case by RNA-Seq of PBMCs. The inflammatory patients (n = 3) clustered into a subset with an inflammatory Th1/Th17 signature and the non-inflammatory patients (n = 7) into another subset with a B cell signature. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700124PMC
January 2016
20 Reads

Atrophy and lower regional perfusion of temporo-parietal brain areas are correlated with impairment in memory performances and increase of EEG upper alpha power in prodromal Alzheimer's disease.

Am J Neurodegener Dis 2015 10;4(1):13-27. Epub 2015 Sep 10.

IRCCS S. Giovanni di Dio Fatebenefratelli Brescia, Italy.

Background: Temporo-parietal cortex thinning is associated with mild cognitive impairment (MCI) due to Alzheimer's disease (AD). The increase of the EEG upper/low alpha power ratio has been associated with MCI due to AD subjects and to the atrophy of temporo-parietal brain areas. Moreover, subjects with a higher alpha3/alpha2 frequency power ratio showed lower brain perfusion than in the low alpha3/alpha2 group. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4568770PMC
September 2015
1 Read

Omental transplantation for neuroendocrinological disorders.

Authors:
Hernando Rafael

Am J Neurodegener Dis 2015 10;4(1):1-12. Epub 2015 Sep 10.

Academia Peruana de Cirugía Lima Peru.

Neurosurgical evidences show that the aging process is initiated between 25 to 30 years of age, in the arcuate nucleus of the hypothalamus. Likewise, experimental and neurosurgical findings indicate that the progressive ischemia in the arcuate nucleus and adjacent nuclei are responsibles at the onset of obesity and, type 2 diabetes mellitus in adults, and essential arterial hypertension (EAH). On the contrary, an omental transplantation on the optic chiasma, carotid bifurcation and anterior perforated space can provoke rejuvenation, gradual loss of body weight, decrease or normalization of hyperglycemia and normalization of EAH; all of them, due to revascularization of the hypothalamic nuclei. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4568769PMC
September 2015

Select small nucleolar RNAs in blood components as novel biomarkers for improved identification of comorbid traumatic brain injury and post-traumatic stress disorder in veterans of the conflicts in Afghanistan and Iraq.

Am J Neurodegener Dis 2014 5;3(3):170-81. Epub 2014 Dec 5.

Department of Neurology, Icahn School of Medicine at Mount Sinai New York, USA ; Neurology Service, James J. Peters Department of Veterans Affairs Medical Center Bronx, New York, USA ; Geriatric Research and Clinical Center, James J. Peter Veterans Affairs Medical Center Bronx, NY, USA.

Background: The present study was designed to validate the ability of our recently identified set of small noncoding RNA candidate mild traumatic brain injury (mTBI) biomarkers to diagnose mTBI in the presence or absence of post-traumatic stress disorder (PTSD) comorbidity. Using qPCR, we explored the regulation of the candidate biomarkers in peripheral blood mononuclear cells (PBMC) from 58 veterans.

Results: We confirmed that 4 small nucleolar RNAs (snoRNAs), ACA48, U35, U55, and U83A, are significantly down-regulated in PBMC from veterans with mTBI and PTSD compared to non-TBI, control subjects with PTSD only. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299721PMC
January 2015
7 Reads

Validation of an Alzheimer's disease assessment battery in Asian participants with mild to moderate Alzheimer's disease.

Am J Neurodegener Dis 2014 5;3(3):158-69. Epub 2014 Dec 5.

Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, NV; Cleveland, OH: Weston, FL, USA.

There is a lack of validated tools for assessing Alzheimer's disease (AD) across Asia. This study evaluates the psychometric properties of the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), Disability Assessment for Dementia (DAD), and Neuropsychological Test Battery (NTB) in Asian participants. Participants with mild to moderate AD (n=251) and healthy controls (n=51) from Mainland China, Taiwan, Singapore, Hong Kong, and South Korea completed selected instruments at several time points. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299719PMC
January 2015
12 Reads

No reactivation of JCV and CMV infections in the temporal cortex and cerebellum of sporadic Creutzfeldt-Jakob disease patients.

Am J Neurodegener Dis 2014 5;3(3):152-7. Epub 2014 Dec 5.

Institute of Neuropathology, University Medical Center Hamburg-Eppendorf Hamburg, Germany.

Sporadic Creutzfeldt-Jakob disease (sCJD) is characterized by great phenotypic variability regarding clinical course and neuropathology. The most prominent disease modifiers are a polymorphism in Codon 129 of the prion protein gene and conformational variations of the misfolded prion protein. The cellular form of the prion protein restricts replication of viruses and may be involved in viral host defense, and viral infections influence the presentation and neuropathology in prion diseased mice. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299723PMC
January 2015
7 Reads

Comparison of two methods for the analysis of CSF Aβ and tau in the diagnosis of Alzheimer's disease.

Am J Neurodegener Dis 2014 5;3(3):143-51. Epub 2014 Dec 5.

Neurodegenerative Disorders Research Pty Ltd 4 Lawrence Ave, West Perth, Western Australia ; School of Medicine and Pharmacology, The University of Western Australia Nedlands, Western Australia.

Introduction: Biomarkers represent a promising adjunct to clinical techniques in the diagnosis of Alzheimer's Disease (AD) and other neurodegenerative diseases. At present, the potential of cerebrospinal fluid (CSF) biomarkers in diagnosing AD has been suggested but the degree of clinical utility is yet to be defined due to variability between studies. In this paper we compare the performance of two cerebrospinal fluid assay methods in predicting clinically diagnosed AD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299722PMC
January 2015
4 Reads

Age-induced reduction of autophagy-related gene expression is associated with onset of Alzheimer's disease.

Am J Neurodegener Dis 2014 5;3(3):134-42. Epub 2014 Dec 5.

Animal Models of Aging, CAMD, National Center for Geriatrics and Gerontology Obu, Aichi, Japan.

Aging is a major risk factor for Alzheimer's disease (AD). Aggregation of amyloid beta (Aβ) in cerebral cortex and hippocampus is a hallmark of AD. Many factors have been identified as causative elements for onset and progression of AD; for instance, tau seems to mediate the neuronal toxicity of Aβ, and downregulation of macroautophagy (autophagy) is thought to be a causative element of AD pathology. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299720PMC
January 2015
2 Reads

Neuropathological and biochemical assessments of an Alzheimer's disease patient treated with the γ-secretase inhibitor semagacestat.

Am J Neurodegener Dis 2014 5;3(3):115-33. Epub 2014 Dec 5.

Laboratory for Neuropathology, Banner Sun Health Research Institute 10515 W. Santa Fe Dr., Sun City, AZ 85351.

Amyloid deposition has been implicated as the key determinant of Alzheimer's disease (AD) pathogenesis. Interventions to antagonize amyloid accumulation and mitigate dementia are now under active investigation. We conducted a combined clinical, biochemical and neuropathological assessment of a participant in a clinical trial of the γ-secretase inhibitor, semagacestat. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299724PMC
January 2015
17 Reads

Cerebral hypometabolism and grey matter density in MAPT intron 10 +3 mutation carriers.

Am J Neurodegener Dis 2014 5;3(3):103-14. Epub 2014 Dec 5.

Indiana Alzheimer Disease Center, Indiana University School of Medicine Indianapolis, IN, USA ; Department of Pathology and Laboratory Medicine, Indiana University School of Medicine Indianapolis, IN, USA.

Multiple systems tauopathy with presenile dementia (MSTD), a form of frontotemporal dementia with parkinsonism-17 with tau inclusions (FTDP-17T), is a neurodegenerative disorder caused by an (a) to (g) transition at position +3 of intron 10 of the microtubule associated protein tau (MAPT) gene. The mutation causes overexpression of 4 repeat (4R) tau isoforms with increased 4R/3R ratio leading to neurodegeneration. Clinically, these patients primarily present with behavioral variant FTD (bvFTD) and show disinhibition, disordered social comportment, and impaired executive function, memory, and speech. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299725PMC
January 2015
14 Reads
1 Citation

Optineurin immunoreactivity in neuronal and glial intranuclear inclusions in adult-onset neuronal intranuclear inclusion disease.

Am J Neurodegener Dis 2014 6;3(2):93-102. Epub 2014 Sep 6.

Department of Neuroscience, Mayo Clinic 4500 San Pablo Road, Jacksonville, FL 32224, USA.

Optineurin (OPTN) is a multifunctional protein involved in cellular morphogenesis, vesicle trafficking, maintenance of the Golgi complex, and transcription activation through its interactions with the Rab8, myosin 6 (MYO6), huntingtin. Recently, OPTN immunoreactivity has been reported in intranuclear inclusions in patients with neuronal intranuclear inclusions disease (NIID). Other studies have shown that the RNA-binding protein, fused in sarcoma (FUS), is a component of intranuclear inclusions in NIID. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162590PMC
September 2014
2 Reads

Somatic complaints in frontotemporal dementia.

Am J Neurodegener Dis 2014 6;3(2):84-92. Epub 2014 Sep 6.

Section of Geriatric Psychiatry, Department of Clinical Sciences, Lund University Klinikgatan 22, Lund SE-221 85, Sweden.

Frontotemporal dementia (FTD) is associated with a broad spectrum of clinical characteristics. The objective of this study was to analyze the prevalence of unexplained somatic complaints in neuropathologically verified FTD. We also examined whether the somatic presentations correlated with protein pathology or regional brain pathology and if the patients with these somatic features showed more depressive traits. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162589PMC
September 2014
2 Reads

Alpha rhythm oscillations and MMSE scores are differently modified by transdermal or oral rivastigmine in patients with Alzheimer's disease.

Authors:
Davide V Moretti

Am J Neurodegener Dis 2014 6;3(2):72-83. Epub 2014 Sep 6.

Scientific Institute for Research and Care (IRCCS) of Alzheimer's and Psychiatric Diseases, S. Giovanni Di Dio, Fatebenefratelli Brescia, Italy.

Background: Alzheimer's disease (AD) is the most common cause of dementia in older patients. Rivastigmine, a reversible cholinesterase inhibitor, has been shown to improve the clinical manifestations of AD by delaying the breakdown of acetylcholine (ACh) released into synaptic clefts. Moreover, there is evidence that ACh modulates EEG alpha frequency. Read More

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September 2014
3 Reads

Greater loss of von Economo neurons than loss of layer II and III neurons in behavioral variant frontotemporal dementia.

Am J Neurodegener Dis 2014 6;3(2):64-71. Epub 2014 Sep 6.

Division of Oncology and Pathology, Department of Clinical Sciences, Lund University Lund, Sweden.

Previous studies have shown a selective reduction of von Economo neurons (VENs) in behavioral variant frontotemporal dementia (bvFTD). However, the alleged selectivity rests on the comparison between VENs and other neurons in cortical layer V, while it has been established that neurons in the superficial cortical layers (I-III) are particularly affected in bvFTD. The purpose of this study was to examine loss the loss of VENs in comparison with that of non-VEN-neurons of superficial cortical layers. Read More

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September 2014
4 Reads

Omental transplantation for neurodegenerative diseases.

Authors:
Hernando Rafael

Am J Neurodegener Dis 2014 6;3(2):50-63. Epub 2014 Sep 6.

Academia Peruana de Cirugía Lima, Peru.

Up to date, almost all researchers consider that there is still no effective therapy for neurodegenerative diseases (NDDs) and therefore, these diseases are incurable. However, since May 1998, we know that a progressive ischemia in the medial temporal lobes and subcommissural regions can cause Alzheimer's disease; because, in contrast to this, its revascularization by means of omental tissue can cure or improve this disease. Likewise we observed that the aging process, Huntington's disease, Parkinson's disease, and Amyotrophic lateral sclerosis; all of them are of ischemic origin caused by cerebral atherosclerosis, associated with vascular anomalies and/or environmental chemicals. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4162586PMC
September 2014

Neuropathologic correlates of trial-related instruments for Alzheimer's disease.

Am J Neurodegener Dis 2014 28;3(1):45-9. Epub 2014 Mar 28.

Department of Pathology & Laboratory Medicine (Neuropathology), The Mary S Easton Center for Alzheimer's Disease Research at The David Geffen School of Medicine at UCLA Los Angeles, CA, USA.

To advance disease-modifying therapies, it is critical to understand the relationship between the neuropathological changes of Alzheimer's Disease (AD) and the clinical measures used in therapeutic trials. We reviewed neuropathologically proven cases of AD from the National Alzheimer's Coordinating Center (NACC) and examined correlations between neuropathological changes and clinical-trial related instruments collected as part of the Uniform Dataset (UDS). We explored the relationships between neurofibrillary tangles, neuritic plaques, and total pathology burden with immediate and delayed recall, Clinical Dementia Rating-Sum of Boxes, Functional Activity Questionnaire, Neuropsychiatric Inventory Questionnaire, and Mini-Mental State Examination scores. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986610PMC
April 2014
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Identification of microRNAs involved in Alzheimer's progression using a rabbit model of the disease.

Am J Neurodegener Dis 2014 28;3(1):33-44. Epub 2014 Mar 28.

Department of Pharmacology, Physiology and Therapeutics, School of Medicine and Health Sciences, University of North Dakota Grand Forks, ND 58202, USA.

Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by the presence of extracellular plaques of β-amyloid peptides and intracellular tangles of hyperphosphorylated tau proteins in the brain. The vast majority of cases are late onset AD (LOAD), which are genetically heterogeneous and occur sporadically. High blood cholesterol is suggested to be a risk factor for this disease. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986609PMC
April 2014
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Development, appraisal, validation and implementation of a consensus protocol for the assessment of cerebral amyloid angiopathy in post-mortem brain tissue.

Am J Neurodegener Dis 2014 28;3(1):19-32. Epub 2014 Mar 28.

Dementia Research Group, School of Clinical Sciences, University of Bristol,Frenchay Hospital UK.

In a collaboration involving 11 groups with research interests in cerebral amyloid angiopathy (CAA), we used a two-stage process to develop and in turn validate a new consensus protocol and scoring scheme for the assessment of CAA and associated vasculopathic abnormalities in post-mortem brain tissue. Stage one used an iterative Delphi-style survey to develop the consensus protocol. The resultant scoring scheme was tested on a series of digital images and paraffin sections that were circulated blind to a number of scorers. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986608PMC
April 2014
13 Reads

C9ORF72 hexanucleotide repeats in behavioral and motor neuron disease: clinical heterogeneity and pathological diversity.

Am J Neurodegener Dis 2014 28;3(1):1-18. Epub 2014 Mar 28.

Department of Neurology, University of California San Francisco, CA, USA.

Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia (FTD), a predominantly behavioral disease, and amyotrophic lateral sclerosis (ALS), a disease of motor neurons. The primary objectives of this review are to highlight the clinical heterogeneity associated with C9ORF72 pathogenic expansion and identify potential molecular mechanisms underlying selective vulnerability of distinct neural populations. The proposed mechanisms by which C9ORF72 expansion causes behavioral and motor neuron disease highlight the emerging role of impaired RNA and protein homeostasis in a spectrum of neurodegeneration and strengthen the biological connection between FTD and ALS. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986607PMC

Differences between early and late onset Alzheimer's disease.

Am J Neurodegener Dis 2013 29;2(4):300-6. Epub 2013 Nov 29.

Neurodegenerative Disorders Research Pty Ltd 185 York Street, Subiaco, Perth, Western Australia 6008.

Previous studies comparing early-onset Alzheimer's disease (EOAD) and late-onset AD (LOAD) have been limited by cross-sectional design and a focus on isolated clinical variables. This study aims to explore differentials in clinical features between EOAD and LOAD and to examine longitudinally trends in cognitive function. Data from 3,747 subjects with AD from C-Path Online Data Repository was used to compare demographics, body mass index (BMI), mean arterial pressure (MAP), biochemistry and cognitive assessments, including mini-mental state examination (MMSE) and Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-Cog), between EOAD and LOAD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852569PMC
December 2013
1 Read

GWAS risk factors in Parkinson's disease: LRRK2 coding variation and genetic interaction with PARK16.

Am J Neurodegener Dis 2013 29;2(4):287-99. Epub 2013 Nov 29.

Department of Neuroscience, Mayo Clinic Jacksonville, Florida, USA.

Parkinson's disease (PD) is a multifactorial movement disorder characterized by progressive neurodegeneration. Genome-wide association studies (GWAS) have nominated over fifteen distinct loci associated with risk of PD, however the biological mechanisms by which these loci influence disease risk are mostly unknown. GWAS are only the first step in the identification of disease genes: the specific causal variants responsible for the risk within the associated loci and the interactions between them must be identified to fully comprehend their impact on the development of PD. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852568PMC
December 2013
8 Reads

Frontotemporal dementia with a C9ORF72 expansion in a Swedish family: clinical and neuropathological characteristics.

Am J Neurodegener Dis 2013 29;2(4):276-86. Epub 2013 Nov 29.

Section of Geriatric Psychiatry, Department of Clinical Sciences, Lund University Klinikgatan 22, Lund SE-221 85, Sweden.

Background: In 2011 the C9ORF72 repeat expansion was identified as the most frequent genetic mutation underlying FTD and ALS. The main aim of this study was to investigate clinical characteristics in a large C9ORF72-positive FTD family, and to compare these with the neuropathological findings.

Methods: The clinical records of 12 related FTD patients were thoroughly evaluated. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852567PMC
December 2013
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Diversity of pathological features other than Lewy bodies in familial Parkinson's disease due to SNCA mutations.

Am J Neurodegener Dis 2013 29;2(4):266-75. Epub 2013 Nov 29.

Departments of Neuroscience, Mayo Clinic Jacksonville, FL, USA ; Current address: Hiroshige Fujishiro, Juntendo University School of Medicine Tokyo, Japan.

The clinical features of the genetically determined forms of familial Parkinson's disease (PD) have been described in multiple reports, but there have been few comparative neuropathologic studies. Five familial PD cases, with mutations in SNCA, were matched for age, sex, and Alzheimer type pathology with sporadic PD cases. Immunohistochemistry for phospho-tau and α-synuclein was performed in 8 brain regions. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852566PMC
December 2013
2 Reads

ER-stress in Alzheimer's disease: turning the scale?

Am J Neurodegener Dis 2013 Nov 29;2(4):247-65. Epub 2013 Nov 29.

Department of Psychiatry and Psychotherapy, Clinical Research Group, University Medical Centre Johannes Gutenberg-University Mainz Untere Zahlbacher Str. 8, D-55131 Mainz, Germany.

Pathogenic mechanisms of Alzheimer's disease (AD) are intensely investigated as it is the most common form of dementia and burdens society by its costs and social demands. While key molecules such as A-beta peptides and tau have been identified decades ago, it is still enigmatic what drives the disease in its sporadic manifestation. Synthesis of A-beta peptides as well as phosphorylation of tau proteins comprise normal cellular functions and occur in principle in the healthy as well as in dementia-affected persons. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852565PMC
November 2013

Aging, circadian rhythms and depressive disorders: a review.

Am J Neurodegener Dis 2013 Nov 29;2(4):228-46. Epub 2013 Nov 29.

Faculty of Medicine, University of Porto Portugal.

Introduction: Aging is typically associated with impairing behavioral patterns that are frequently and inappropriately seen as normal. Circadian rhythm changes and depressive disorders have been increasingly proposed as the two main overlapping and interpenetrating changes that take place in older age. This study aims to review the state of the art on the subject concerning epidemiology, pathophysiological mechanism, clinical findings and relevance, as well as available treatment options. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852564PMC
November 2013
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Dopaminergic innervation of the human subventricular zone: a comparison between Huntington's chorea and Parkinson's disease.

Am J Neurodegener Dis 2013 18;2(3):221-7. Epub 2013 Sep 18.

Centre de recherche de l'Institut universitaire en santé mentale de Québec, Department of Psychiatry and Neuroscience, Faculty of Medicine, Université Laval Quebec City, QC, Canada.

The subventricular zone retains its neurogenic capacity throughout life and, as such, is often considered a potential source for endogenous repair in neurodegenerative disorders. Because dopamine is believed to stimulate adult neurogenesis, we looked for possible variations in the dopaminergic innervation of the subventricular zone between cases of Huntington's chorea and Parkinson's diseases. Antibodies against tyrosine hydroxylase (TH) and proliferating cell nuclear antigen (PCNA) were used as specific markers of dopaminergic axons and cell proliferating activity, respectively. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3783834PMC
October 2013
4 Reads