Neurofilament proteins NF-L, NF-M and NF-H in brain of patients with Down syndrome and Alzheimer's disease

Bajo, M.; Yoo, Byong Chul; Cairns, Nigel J.; Gratzer, M.; Lubec, Gert

doi:10.1007/s007260170015

Cited by 29 publications

(17 citation statements)

References 19 publications

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“…The results regarding staining of neurofilaments in AD are somewhat conflicting, because the studies have used different methods [8,10,11]. One previous study reported decreased staining of NFL and increased staining of NFH in AD [10]. Another study found that antibodies against neurofilaments stained neurofibrillary tangles as well as neuritic plaques [8], a finding not convincingly attested by the present results.…”

Section: Discussioncontrasting

confidence: 55%

“…Another study found spheroidal enlargements of presynaptic terminals that were immunopositive for the cytoskeletal tau proteins, NFH, and beta-tubulin [11]. The results regarding staining of neurofilaments in AD are somewhat conflicting, because the studies have used different methods [8,10,11]. One previous study reported decreased staining of NFL and increased staining of NFH in AD [10].…”

Section: Discussionmentioning

confidence: 95%

“…In AD, antibodies against neurofilament proteins have been reported to stain neurofibrillary tangles [8,9], however with variable intensity [10]. In FTD, antibodies against NFH and tau have been found to stain neuronal swellings in the neuropil [11].…”

Section: Introductionmentioning

confidence: 99%

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Negative Neurofilament Light and Tau Immunostaining in Frontotemporal Dementia

Sjögren

Englund²

2004

Dement Geriatr Cogn Disord

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We investigated the immunohistochemical stainability of phosphorylated tau and the light (NFL), intermediate (NFM), and heavy (NFH) neurofilament proteins in postmortem brain tissue from 8 patients with frontotemporal dementia (FTD), for comparison with 6 patients with Alzheimer’s disease (AD), and 6 normal controls. In the FTD group, the neuropathological diagnosis was pure frontal-lobe degeneration of non-Alzheimer type (FLD) in 6 cases and in the remaining 2 cases mixed FLD-AD and frontal AD, respectively. The staining for tau was negative in 5 of the FLD cases and faintly positive in 1, but positive in all AD cases. The antibodies against NFM and NFH stained positive in FLD, AD, and controls, whereas the staining for NFL was negative in all FLD cases and positive in 1 AD case and in the controls. These findings regarding NFL and tau staining may be useful in the differential diagnosis of FLD and AD.

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Section: Discussioncontrasting

confidence: 55%

Section: Discussionmentioning

confidence: 95%

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Negative Neurofilament Light and Tau Immunostaining in Frontotemporal Dementia

Sjögren

Englund²

2004

Dement Geriatr Cogn Disord

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“…In addition NFs are involved in cytoskeleton organization, neurogenesis and supports the neuronal architecture in the brain [92]. The protein levels of NF-L in brains of AD, Down syndrome, and ALS patients is signsificantly decreased [8,9], suggesting that normal NF-L expression could be critical to central nervous system (CNS) function. Oxidation or nitration of neurofilament (NF) proteins transform the α-helix secondary structure to β-sheet and random coil conformations, destabilizing the interactions between the NF proteins and resulting in axonal damage [41] and CNS dysfunction.…”

Section: Maintenance and Stabilization Of The Integrity Of The Cell Smentioning

confidence: 99%

Proteomic identification of brain proteins in the canine model of human aging following a long-term treatment with antioxidants and a program of behavioral enrichment: Relevance to Alzheimer's disease

Opii

Joshi

Head

et al. 2008

Neurobiology of Aging

175

135

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Aging and age-related disorders such as Alzheimer's disease (AD) are usually accompanied by oxidative stress as one of the main mechanisms contributing to neurodegeneration and cognitive decline. Aging canines develop cognitive dysfunction and neuropathology similar to those seen in humans, and the use of antioxidants results in reductions in oxidative damage and in improvement in cognitive function in this canine model of human aging. In the present study, the effect of a longterm treatment with an antioxidant fortified diet and a program of behavioral enrichment on oxidative damage was studied in aged canines. To identify the neurobiological mechanisms underlying these treatment effects, the parietal cortex from 23 beagle dogs (8.1-12.4 years) were treated for 2.8 years in one of four treatment groups: i.e., control food-control behavioral enrichment (CC); control food -behavioral enrichment (CE); antioxidant food-control behavioral enrichment (CA); and enriched environment -antioxidant fortified food (EA). We analyzed the levels of the oxidative stress biomarkers, i.e., protein carbonyls, 3-nitrotyroine (3NT), and the lipid peroxidation product, 4- Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeurobiol Aging. Author manuscript; available in PMC 2009 January 1. Published in final edited form as:Neurobiol Aging. 2008 January ; 29(1): 51-70. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript hydroxynonenal (HNE), and observed a decrease in their levels on all treatments when compared to control, with the most significant effects found in the combined treatment, EA. Since EA treatment was most effective, we also carried out a comparative proteomics study to identify specific brain proteins that were differentially expressed and used a parallel redox proteomics approach to identify specific brain proteins that were less oxidized following EA. The specific protein carbonyl levels of glutamate dehydrogenase [NAD (P)], glyceraldehyde-3-phosphate dehydrogenase (GAPDH), α-enolase, neurofilament triplet L protein, glutathione S-transferase (GST) and fascin actin bundling protein were significantly reduced in brain of EA-treated dogs compared to control. We also observed significant increases in expression of Cu/Zn superoxide dismutase, fructose-bisphosphate aldolase C, creatine kinase, glutamate dehydrogenase and glyceraldehyde-3-phosphate dehydrogenase. The increased expression of these proteins and in particular Cu/Zn SOD correlated with improved cognitive function. In addition, there was a significant increas...

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“…Drebrin's reduced levels may mean deterioration of dendritic spine structure [157]. Reduced expression was also observed for the structural constituent of the cytoskeleton neurofilament L [158] and for stathmin [144]. In the fetal DS brain, reduced levels were found for actinrelated protein complex 2/3 20 kDa and coronin-like protein p57 [159].…”

Section: Structural Proteinsmentioning

confidence: 99%

Proteomics‐driven progress in neurodegeneration research

Fountoulakis

Κοσσίδα

2006

Electrophoresis

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Proteomics-driven progress in neurodegeneration researchProteomics technologies have been widely used in the investigation of neurodegenerative and psychiatric disorders, and in particular in the detection of differences between healthy individuals and patients suffering from such diseases. Thus, brain and cerebrospinal fluid (CSF) samples from patients with Alzheimer's disease, Down syndrome, Pick's disease, Parkinson's disease, schizophrenia, and other disorders as well as brain and CSF from animals serving as models of neurological disorders have been analyzed by proteomics. 2-DE followed by MALDI-TOF-MS has been mainly applied as this proteomics approach provides the possibility of convenient quantification of protein levels and detection of post-translational modifications. About 330 unique proteins with deranged levels and modifications have been detected by proteomics approaches to be related to neurodegeneration and psychiatric disorders. They are mainly involved in metabolism pathways, cytoskeleton formation, signal transduction, guidance, detoxification, transport, and conformational changes. In this article, we provide a summary of the major contributions of proteomics technologies in the study of neurodegenerative and psychiatric diseases, in particular, in the detection of changes in protein levels and modifications related to these disorders. IntroductionNeurodegeneration is a major hallmark of a series of genetic and acquired disorders of the central nervous system (CNS), like Alzheimer's disease (AD), Down syndrome (DS), Pick's disease, Creutzfeldt-Jakob disease (CJD), and Parkinson's disease, which result in severe cognitive and motor deficits. A common characteristic of these diseases is that they are multifactorial.Their molecular basis is unknown and individual biomarkers are not reliable. Genomics and proteomics approaches have been applied to obtain a better understanding of neurodegeneration and psychiatric disorders. Genomics has been used to map and identify genes that are mutated in a wide variety of such disorders, like presenilins in AD. Next to genomics, which only provides a partial view of the biological problem, proteomics is widely used in clinical diagnosis as well and many changes in protein levels associated with specific diseases have been identified [1,2].Proteomics is a technology-driven science that studies the proteins of the various biological systems, their structures, interactions, post-translational modifications, and in particular the changes in their levels and modifications, which are the result of specific diseases or are induced by external factors.

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Neurofilament proteins NF-L, NF-M and NF-H in brain of patients with Down syndrome and Alzheimer's disease

Cited by 29 publications

References 19 publications

Negative Neurofilament Light and Tau Immunostaining in Frontotemporal Dementia

Negative Neurofilament Light and Tau Immunostaining in Frontotemporal Dementia

Proteomic identification of brain proteins in the canine model of human aging following a long-term treatment with antioxidants and a program of behavioral enrichment: Relevance to Alzheimer's disease

Proteomics‐driven progress in neurodegeneration research

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