Thalamic metabolism and symptom onset in preclinical Huntington's disease.

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Abstract Text:

A Feigin,C Tang,Y Ma,P Mattis,D Zgaljardic,M Guttman,J S Paulsen,V Dhawan,D Eidelberg,A Feigin,C Tang,Y Ma,P Mattis,D Zgaljardic,M Guttman,J S Paulsen,V Dhawan,D Eidelberg,

The neural basis for the transition from preclinical to symptomatic Huntington's disease (HD) is unknown. We used serial positron emission tomography (PET) imaging in preclinical HD gene carriers (p-HD) to assess the metabolic changes that occur during this period. Twelve p-HD subjects were followed longitudinally with [11C]-raclopride and [18F]-fluorodeoxyglucose PET imaging, with scans at baseline, 18 and 44 months. Progressive declines in striatal D2-receptor binding were correlated with concurrent changes in regional metabolism and in the activity of an HD-related metabolic network. We found that striatal D2 binding declined over time (P < 0.005). The activity of a reproducible HD-related metabolic covariance pattern increased between baseline and 18 months (P < 0.003) but declined at 44 months (P < 0.04). These network changes coincided with progressive declines in striatal and thalamic metabolic activity (P < 0.01). Striatal metabolism was abnormally low at all time points (P < 0.005). By contrast, thalamic metabolism was elevated at baseline (P < 0.01), but fell to subnormal levels in the p-HD subjects who developed symptoms. These findings were confirmed with an MRI-based atrophy correction for each individual PET scan. Increases in network expression and thalamic glucose metabolism may be compensatory for early neuronal losses in p-HD. Declines in these measures may herald the onset of symptoms in gene carriers.

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Publishing Authors By Initials

A Feigin,C Tang,Y Ma,P Mattis,D Zgaljardic,M Guttman,JS Paulsen,V Dhawan,D Eidelberg,A Feigin,C Tang,Y Ma,P Mattis,D Zgaljardic,M Guttman,JS Paulsen,V Dhawan,D Eidelberg,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Brain : a journal of neurology

VOLUME: 130

Page Numbers: 2858-67

Journal Abbreviation: Brain

ISSN: 1460-2156

DAY: 24

MONTH: 09

YEAR: 2007

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 372537

Thalamic metabolism and symptom onset in preclinical Huntington's disease. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Thalamic metabolism and symptom onset in preclinical Huntington's disease. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Thalamic metabolism and symptom onset in preclinical Huntington's disease.

AFFILIATION: Center for Neurosciences, The Feinstein Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, NY 11030, USA.

Country: England

AGENCY: United States NINDS

GRANT: R01 NS 37564

ACRONYM: NS

MEDLINETA: Brain

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Thalamic metabolism and symptom onset in preclinical Huntington's disease Related Publications

• Abnormal metabolic network activity in Parkinson's disease: test-retest reproducibility.
• Abnormal metabolic networks in atypical parkinsonism.
• An examination of executive dysfunction associated with frontostriatal circuitry in Parkinson's disease.
• Callosal and non-callosal connexions between the sensory-motor cortices in cat and monkey.
• Cerebral glucose metabolism and D(2)/D (3) receptor availability in young adults with cannabis dependence measured with positron emission tomography.
• Changes in network activity with the progression of Parkinson's disease.
• Correlates of movement initiation and velocity in Parkinson's disease: A longitudinal PET study.
• Development of electrical activity in the cerebral cortex of the newborn rat.
• Dissociation of metabolic and neurovascular responses to levodopa in the treatment of Parkinson's disease.
• Dopaminergic suppression of brain deactivation responses during sequence learning.
• Functional imaging of cerebral blood flow and glucose metabolism in Parkinson's disease and Huntington's disease.
• Functional imaging of sequence learning in Parkinson's disease.
• Gene transfer therapy for neurodegenerative disorders.
• Habituation of somatosensory evoked potentials in the lemniscal system of the cat.
• Implicit and explicit aspects of sequence learning in pre-symptomatic Huntington's disease.
• Increased cerebellar activation during sequence learning in DYT1 carriers: an equiperformance study.
• Metabolic abnormalities associated with mild cognitive impairment in Parkinson disease.
• Metabolic brain networks associated with cognitive function in Parkinson's disease.
• Metabolic correlates of subthalamic nucleus activity in Parkinson's disease.
• Microstructural white matter changes in primary torsion dystonia.
• Modulation of metabolic brain networks after subthalamic gene therapy for Parkinson's disease.
• Relationship between self-reported apathy and executive dysfunction in nondemented patients with Parkinson disease.
• Spectrum analysis of residual EEG changes following post-natal x-irradiation in rats.
• Subthalamic glutamic acid decarboxylase gene therapy: changes in motor function and cortical metabolism.
• Thalamic metabolism and symptom onset in preclinical Huntington's disease.
• The assessment of neurological systems with functional imaging.
• Thermoelectric freezing stage for serial brain sectioning.
• [Not Available.]
• [Not Available.]
• [Treatment of pain in neoplastic diseases.]