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essential tremor/tyrosine
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Essential tremor is not a neurodegenerative disease.
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The pathophysiology of essential tremor (ET) remains unknown. Standard neuropathological studies have reported no consistent changes but a detailed study found neurodegeneration in all ET cases - 24% demonstrated lower brainstem Lewy body (LB) inclusions and 76% experienced a loss of cerebellar
Brain biochemistry in autopsied patients with essential tremor.
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The pathology of essential tremor is increasingly being studied; however, there are limited studies of biochemical changes in this condition. We studied several candidate biochemical/anatomical systems in the brain stem, striatum, and cerebellum of 23 essential tremor subjects who came to autopsy,
Change in the concentrations of amino acids in CSF and serum of patients with essential tremor.
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The concentrations of amino acids in the cerebrospinal fluid (CSF) (n = 20) and serum (n = 20) taken from patients with essential tremor were measured by HPLC and compared with those of controls (n = 10). Reduced concentrations of some amino acids (asparagine, glutamine, glycine, threonine,
A variant in the HS1-BP3 gene is associated with familial essential tremor.
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BACKGROUND
Genetic linkage studies have identified two susceptibility loci for essential tremor (ET) on chromosomes 3q13 (ETM1) and 2p24.1 (ETM2). Linkage disequilibrium studies in separate population samples from the United States and Singapore suggest an association between ET and loci at
Olfaction and Parkinson's syndromes: its role in differential diagnosis.
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OBJECTIVE
Marked olfactory dysfunction (hyposmia) is a frequent and early abnormality in Parkinson's disease. We review recent advances related to its cause and its clinical relevance with respect to the differential diagnosis of Parkinsonian syndromes.
RESULTS
Marked olfactory dysfunction occurs in
Post mortem studies in Parkinson's disease--is it possible to detect brain areas for specific symptoms?
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Parkinson's disease (PD) is characterized by progressive neuronal loss associated with Lewy bodies in many subcortical nuclei leading to multiple biochemical and pathophysiological changes of clinical relevance. Loss of nigral neurons causing striatal dopamine deficiency is related to both the
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