pantothenate kinase-associated neurodegeneration/amyloid

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Alzheimer's amyloid precursor protein accumulates within axonal swellings in human brain lesions.

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By using a monoclonal antibody and polyclonal antibodies to human beta amyloid precursor protein (APP), we immunohistochemically examined axonal swellings (spheroids). The immunoreactivity of APP was observed in numerous spheroids, which were found around the areas of old cerebral infarctions, in

Non-Alzheimer neurofibrillary tangles show beta-amyloid-like immunoreactivity.

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As well as being a neuropathological hallmark of Alzheimer's disease (AD), neurofibrillary tangles (NFT) are present in the brain in a number of other neurodegenerative conditions. beta-Amyloid (beta/A4) plaque formation is a central event in AD, although recent reports indicate that beta/A4, and

Widespread occurrence of alpha-synuclein/NACP-immunoreactive neuronal inclusions in juvenile and adult-onset Hallervorden-Spatz disease with Lewy bodies.

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Alpha-Synuclein (originally called precursor of the non-Abeta component of Alzheimer's disease amyloid-NACP) is a presynaptic nerve terminal protein and is now known to be a major component of Lewy bodies (LBs) in Parkinson's disease. Previous studies have shown that LBs are occasionally found in

Ultrastructure and immunoreactivity of dystrophic axons indicate a different pathogenesis of Hallervorden-Spatz disease and infantile neuroaxonal dystrophy.

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An immunohistochemical and ultrastructural analysis of dystrophic axons (DAs) in the brain and peripheral nerve of a patient with familial infantile neuroaxonal dystrophy (INAD) and in the brain of a patient with familial Hallervorden-Spatz Disease (HSD) revealed prevalent membrano-tubular or

Coexistence of TDP-43 and tau pathology in neurodegeneration with brain iron accumulation type 1 (NBIA-1, formerly Hallervorden-Spatz syndrome).

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We report here an autopsy case of sporadic adult-onset Hallervorden-Spatz syndrome, also known as neurodegeneration with brain iron accumulation type 1 (NBIA1), without hereditary burden. A 49-year-old woman died after a 27-year disease course. At the age of 22, she suffered from akinesia, resting

Adult onset Hallervorden-Spatz disease with neurofibrillary pathology. A discrete clinicopathological entity.

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Three adults with progressive cognitive decline and extrapyramidal dysfunction were studied. They were all mentally retarded women without known chromosomal abnormalities, ranging in age at the time of onset from 31 to 42 yrs with an average duration of illness of 6 yrs. Neurological signs were

Juvenile-onset generalized neuroaxonal dystrophy (Hallervorden-Spatz disease) with diffuse neurofibrillary and lewy body pathology.

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We describe an unusual case of Hallervorden-Spatz disease (HSD). After presenting with limb rigidospasticity at the age of 9 years, our patient developed progressive dementia, spastic tetraparesis and myoclonic movements, leading to akinetic mutism. He died of pneumonia at the age of 39 years.

Lewy body in neurodegeneration with brain iron accumulation type 1 is immunoreactive for alpha-synuclein.

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In familial PD, a mutation of the alpha-synuclein gene has been identified. Alpha-synuclein also was revealed in Lewy bodies in idiopathic PD. Lewy bodies in neurodegeneration with brain iron accumulation type 1 (NBIA 1; Hallervorden-Spatz syndrome) were found to show immunostaining for

Neuropathology of synuclein aggregates.

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Beginning with the isolation of the fragment of alpha-synuclein (alpha-syn) known as the non-Abeta component of amyloid plaques (NAC peptide) from Alzheimer's disease (AD) brains, alpha-syn has been increasingly implicated in the pathogenesis of neurodegenerative diseases, which now are classified

Transgenic models of alpha-synuclein pathology: past, present, and future.

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Accumulation and toxic conversion to protofibrils of alpha-synuclein has been associated with neurological disorders such as Parkinson's disease (PD), Lewy body disease, multiple system atrophy, neurodegeneration with brain iron accumulation type 1, and Alzheimer's disease. In recent years, modeling

Neuropathological spectrum of synucleinopathies.

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Synucleinopathies comprise a diverse group of neurodegenerative proteinopathies that share common pathological lesions composed of aggregates of conformational and posttranslational modifications of alpha-synuclein in selected populations of neurons and glia. Abnormal filamentous aggregates of

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