Neurofilament proteins in neurodegenerative diseases

Liu, Q.; Xie, Fei; Siedlak, Sandra L.; Nunomura, Akihiko; Honda, Kazuo; Moreira, Paula I.; Zhua, X.; Smith, Mark A.; Perry, George

doi:10.1007/s00018-004-4268-8

Cited by 149 publications

(123 citation statements)

References 208 publications

(284 reference statements)

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“…In CNS injury, elevated expression of GFAP was associated with astrocyte activation, modulated by TGF-␤1, during neural responses to injury (221). NFs, which are comprised of neurofilament light (NF-L), neurofilament medium (NF-M), and neurofilament heavy (NF-H) subunits, are intermediate filaments found specifically in neurons and are considered to convey tensile strength, structural rigidity, and intracellular transport guidance to dendrites and axons, while abnormal accumulation of NF-L is detected in AD (216,222). Evidence also indicates that some enzymes, such as tTG and ubiquitin, are potent mediators of the pathogenesis of AD.…”

Section: Cerebral Toxocariasis Versus Alzheimer's Disease: a Silent Pmentioning

confidence: 99%

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

et al. 2015

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SUMMARY Toxocara canis and T. cati are highly prevalent nematode infections of the intestines of dogs and cats. In paratenic hosts, larvae do not mature in the intestine but instead migrate through the somatic tissues and organs of the body. The presence of these migrating larvae can contribute to pathology. Toxocara larvae can invade the brains of humans, and while case descriptions of cerebral toxocariasis are historically rare, improved diagnosis and greater awareness have contributed to increased detection. Despite this, cerebral or neurological toxocariasis (NT) remains a poorly understood phenomenon. Furthermore, our understanding of cognitive deficits due to toxocariasis in human populations remains particularly deficient. Recent data describe an enhanced expression of biomarkers associated with brain injury, such as GFAP, AβPP, transforming growth factor β1 (TGF-β1), NF-L, S100B, tTG, and p-tau, in mice receiving even low doses of Toxocara ova. Finally, this review outlines a hypothesis to explore the relationship between the presence of T. canis larvae in the brain and the progression of Alzheimer's disease (AD) due to enhanced AD-associated neurodegenerative biomarker expression.

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Section: Cerebral Toxocariasis Versus Alzheimer's Disease: a Silent Pmentioning

confidence: 99%

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

et al. 2015

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“…En otras enfermedades neurológicas la patología dendrítica hallada con el método de Golgi se ha correlacionado con pérdida de MAP-2 (21-23). Así mismo, alteraciones en las proteínas NF se han asociado con enfermedades neurodegenerativas (25).…”

Section: Discussionunclassified

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

2007

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Introducción. Los signos neurológicos de la rabia son impresionantes; no obstante, el cerebro infectado sufre apenas cambios histológicos muy sutiles. Objetivo. Estudiar la morfología neuronal mediante la técnica de Golgi, en la corteza cerebral de ratones infectados con el virus de la rabia. Materiales y métodos. Se inocularon ratones con virus silvestre de la rabia (virus 'calle') de origen canino o con virus adaptado (virus 'fijo') de la cepa CVS (challenge virus standard). Los animales se sacrificaron en la fase terminal de la enfermedad y se fijaron por perfusión con paraformaldehído. Los cerebros se procesaron con la técnica de Golgi, se obtuvieron cortes coronales de la corteza, se contaron las neuronas impregnadas en un área de 1 mm 2 , se midió el tamaño de sus cuerpos celulares y se tomaron fotografías en diferentes planos de profundidad. Resultados. Se observaron alteraciones morfológicas notables en el soma y las dendritas de neuronas piramidales, con pérdida acentuada de espinas, en 12,9% de neuronas corticales de animales infectados con virus 'calle' por vía intracerebral; en 8,2% de neuronas de ratones inoculados con este mismo virus por la ruta intramuscular y en 31,8% de neuronas en los animales inoculados con virus 'fijo' por vía intramuscular. Además, en las muestras de material infectado el número de neuronas impregnadas por la técnica de Golgi fue considerablemente menor al observado en las muestras no infectadas. Conclusiones. Estos resultados son evidencia de que el virus de la rabia sí puede inducir daño neuronal estructural. Además, esta infección aparentemente interfiere con los mecanismos de impregnación argéntica del método de Golgi.Palabras clave: rabia, virus de la rabia, corteza cerebral, neuronas, neuroanatomía, técnicas histológicas. Neuronal dentritic morphology alterations in the cerebral cortex of rabies-infected mice: a Golgi studyIntroduction. The neurological signs of rabies are very dramatic. Nevertheless, the infected brain manifests only very subtle histological changes. Objective. The neuronal morphology in the cerebral cortex of rabies-infected mice was examined by means the Golgi technique for detection of neuropathy. Materials and methods. Two groups of mice were inoculated with rabies-one with street virus isolated from an infected dog and the second with fixed CVS (challenge virus standard) virus. At the terminal phase of illness, the animals were sacrificed and fixed for histological staining by perfusion with paraformaldehyde. Next, the brains were treated by the Golgi technique and coronal sections were obtained. Neurons enclosed within 1 mm 2 frames of the frontal cortex sections were counted and the sizes of the cellular bodies were measured. Photographs of several depth levels from the sections were obtained. Results. Cortical pyramidal neurons showed distinctive morphological alterations in the soma and dendrites (including loss of dendritic spines) in 12.9% of cells from intracerebral infectedmice with street virus; in 8.2% of neurons from intramuscular inf...

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“…33 The abnormal accumulation of intermediate filament proteins is a pathological hallmark of many human neurodegenerative diseases, that is, Amyotrophic lateral sclerosis, Parkinson's disease, dementia with Lewy bodies and neuropathies. 33,34 Following their synthesis in the perikaryon, neurofilament proteins are swiftly assembled into filamentous structures and translocated into the axons. 33 The decreased expression of a-internexin in the alcoholic groups is consistent with brain shrinkage and neuronal death and this together with the decline in hNP22 expression indicates that chronic alcohol use has specific effects on the cytoskeleton.…”

Section: Discussionmentioning

confidence: 99%

Differential protein expression in the prefrontal white matter of human alcoholics: a proteomics study

et al. 2005

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Neuroimaging and post-mortem studies indicate that chronic alcohol use induces global changes in brain morphology, such as cortical and subcortical atrophy. Recent studies have shown that frontal lobe structures are specifically susceptible to alcohol-related brain damage and shrinkage in this area is largely due to a loss of white matter. This may explain the high incidence of cognitive dysfunction observed in alcoholics. Using a proteomics-based approach, changes in protein expression in the dorsolateral prefrontal region (BA9) white matter were identified in human alcoholic brains. Protein extracts from the BA9 white matter of 25 human brains (10 controls; eight uncomplicated alcoholics; six alcoholics complicated with hepatic cirrhosis; one reformed alcoholic) were separated using two-dimensional gel electrophoresis. Overall, changes in the relative expression of 60 proteins were identified (Po0.05, ANOVA) in the alcoholic BA9 white matter. In total, 18 protein spots have been identified using MALDI-TOF; including hNP22, a-internexin, transketolase, creatine kinase chain B, ubiquitin carboxy-terminal hydrolase L1 and glyceraldehyde-3-phosphate dehydrogenase. Several of these proteins have been previously implicated in alcohol-related disorders and brain damage. By identifying changes in protein expression in this region from alcoholics, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes white matter damage.

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Neurofilament proteins in neurodegenerative diseases

Cited by 149 publications

References 208 publications

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

Cerebral Toxocariasis: Silent Progression to Neurodegenerative Disorders?

Alteraciones de la morfología dendrítica neuronal en la corteza cerebral de ratones infectados con rabia: un estudio con la técnica de Golgi

Differential protein expression in the prefrontal white matter of human alcoholics: a proteomics study

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