lewy body disease/tyrosine

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Degeneration of tyrosine hydroxylase-immunoreactive neurons in the cerebral cortex and hippocampus of patients with dementia with Lewy bodies.

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We immunohistochemically investigated the degeneration of tyrosine hydroxylase (TH)-positive neurons in the cerebral cortex and hippocampus of dementia with Lewy bodies (DLB) brains. TH-positive neurons in the cerebral cortex and hippocampus were decreased in number, and were rarely associated with

Neuropathological characterization of Lemur tyrosine kinase 2 (LMTK2) in Alzheimer's disease and neocortical Lewy body disease.

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Alzheimer's disease (AD) and neocortical Lewy body disease (LBD) are the most common neurodegenerative dementias, with no available curative treatment. Elucidating pathomechanism and identifying novel therapeutic targets are of paramount importance. Lemur tyrosine kinase 2 (LMTK2) is involved in

Reduced striatal tyrosine hydroxylase in incidental Lewy body disease.

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Incidental Lewy body disease (ILBD) is the term used when Lewy bodies are found in the nervous system of subjects without clinically documented parkinsonism or dementia. The prevalence of ILBD in the elderly population has been estimated at between 3.8 and 30%, depending on subject age and

Transgenic mice overexpressing tyrosine-to-cysteine mutant human alpha-synuclein: a progressive neurodegenerative model of diffuse Lewy body disease.

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Abnormal aggregation of human alpha-synuclein in Lewy bodies and Lewy neurites is a pathological hallmark of Parkinson disease and dementia with Lewy bodies. Studies have shown that oxidation and nitration of alpha-synuclein lead to the formation of stable dimers and oligomers through dityrosine

Investigating the Presence of Doubly-phosphorylated α-Synuclein at Tyrosine 125 and Serine 129 In Idiopathic Lewy Body Diseases.

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Aggregation of the protein α-synuclein (α-syn) into insoluble intracellular assemblies termed Lewy bodies (LBs) is thought to be a critical pathogenic event in LB diseases such as Parkinson's disease and dementia with LBs. In LB diseases, the majority of α-syn is phosphorylated at serine 129

Association of MAPT H1 subhaplotypes with neuropathology of lewy body disease.

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Genetic variation at the microtubule-associated protein tau locus is associated with clinical parkinsonism. However, it is unclear as to whether microtubule-associated protein tau H1 subhaplotypes are associated with the burden of neuropathological features of Lewy body

Altered Expression Patterns of Inflammation-Associated and Trophic Molecules in Substantia Nigra and Striatum Brain Samples from Parkinson's Disease, Incidental Lewy Body Disease and Normal Control Cases.

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Evidence of inflammation has been consistently associated with pathology in Parkinson's disease (PD)-affected brains, and has been suggested as a causative factor. Dopaminergic neurons in the substantia nigra (SN) pars compacta, whose loss results in the clinical symptoms associated with PD, are

A neuropathological study of the disturbance of the nigro-amygdaloid connections in brains from patients with dementia with Lewy bodies.

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We neuropathologically and immunohistochemically investigated characteristics of the central amygdaloid nucleus lesion and its relationship with the substantia nigra lesion in dementia with Lewy bodies (DLB) brains. Nine DLB, four Parkinson's disease (PD) and four Alzheimer-type dementia (ATD) cases

Immunohistochemistry of neuronal inclusions in the cerebral cortex and brain-stem in Lewy body disease.

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Three cases of Lewy body disease were investigated in order to compare the morphological and immunohistochemical characteristics of the neuronal inclusions in the cerebral cortex (CC) and brain-stem (BS). Ultrastructurally, the CC contained intermediate-sized filaments with variable amounts of

Immunoreactivity profile of hippocampal CA2/3 neurites in diffuse Lewy body disease.

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Ubiquitin-immunoreactive dystrophic neurites in the CA2/3 region of the hippocampus are characteristic of diffuse Lewy body disease (DLBD). The origin of dystrophic CA2/3 neurites is unknown, but their extent correlates with the number of cortical Lewy bodies (LBs). To examine the molecular

Clinical and pathological features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies.

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To clarify the features affecting cardiac sympathetic denervation in autopsy-confirmed dementia with Lewy bodies (DLB) patients.Fifty-four autopsy-confirmed DLB patients were enrolled. Tissue samples of the left ventricular anterior wall were immunostained

The nigro-striatal and nigro-amygdaloid pathways undergo different degeneration processes in brains of dementia with Lewy bodies.

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We immunohistochemically investigated the degeneration processes of the nigro-striatal and nigro-amygdaloid pathways and the relationship between the loss of dopaminergic neurons and Lewy bodies (LB) formation in the substantia nigra using 15 autopsied cases of dementia with Lewy bodies (DLB). The

Dopamine cell loss in the periaqueductal gray in multiple system atrophy and Lewy body dementia.

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BACKGROUND Experimental studies indicate that dopaminergic neurons in the ventral periaqueductal gray matter (PAG) are involved in maintenance of wakefulness. Excessive daytime sleepiness (EDS) is a common manifestation of multiple system atrophy (MSA) and dementia with Lewy bodies (DLB) but

Lewy bodies in tyrosine hydroxylase-synthesizing neurons of the human cerebral cortex.

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A population of neurons situated in the human cerebral neocortex contains mRNA coding for tyrosine hydroxylase, the key enzyme for catecholamine biosynthesis. Phosphorylated neurofilament-containing cytoplasmic inclusions occur in these neurons in diffuse Lewy body disease, indicating a tendency for

"Sick-but-not-dead": Multiple paths to catecholamine deficiency in Lewy Body diseases.

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Profound depletion of the catecholamines dopamine and norepinephrine in the brain, heart, or both characterize Lewy body diseases such as Parkinson disease, dementia with Lewy bodies, and pure autonomic failure. Although one might presume that catecholamine deficiency in these disorders results

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