Olfactory and auditory event-related potentials in Huntington's disease.

Wetter, Spencer; Peavy, Guerry M.; Jacobson, Mark W.; Hamilton, Joanne M.; Salmon, David P.; Murphy, Claire

doi:10.1037/0894-4105.19.4.428

Cited by 13 publications

(7 citation statements)

References 66 publications

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“…However, it is now appreciated that htt-induced deficits are more widespread, involving cortex, hippocampus, hypothalamus and olfactory function (Hedreen et al, 1991;Spargo et al, 1993;Murphy et al, 2000;Mitchell et al, 2005;Petersen et al 2005;Wetter et al, 2005). These regions correspond to the specific localization of Bcl11b in the CNS, as described herein, and by others (Leid et al 2004;Arlotta et al 2005;Desplats et al 2006).…”

Section: Discussionsupporting

confidence: 75%

Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease

Desplats

Lambert

Thomas

2008

Neurobiology of Disease

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Transcriptional dysregulation has emerged as a central pathogenic mechanism in Huntington's disease (HD), which is associated with neuropathological changes predominantly in the striatum. Here we demonstrate that expression of Bcl11b (a.k.a. CTIP2), a transcription factor exhibiting highly-enriched localization in adult striatum, is significantly decreased in HD cells, mouse models and human subjects and that overexpression of Bcl11b attenuates toxic effects of mutant huntingtin in cultured striatal neurons. We show that Bcl11b directly activates the proximal promoter regions of striatal-enriched genes and can increase mRNA levels of striatal-expressing genes. We further demonstrate an interaction between Bcl11b and huntingtin protein in cultured cells and brain homogenates from HD R6/1 and YAC72 transgenic mice. We propose that sequestration and/or decreased expression of Bcl11b in HD is responsible, at least in part, for the dysregulation of striatal gene expression observed in HD and may contribute to the specificity of pathology observed in this disease.

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Section: Discussionsupporting

confidence: 75%

Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease

Desplats

Lambert

Thomas

2008

Neurobiology of Disease

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“…Recently, one group of researchers found deficits in olfactory function in gene carriers who were on average 4.7 years from predicted onset of HD (Wetter et al, 2006). In an olfactory event-related potential (ERP) study, Wetter et al (2005) found that HD patients showed latency delays on the cognitive P3 component of the olfactory ERP. Recently, these researchers used the same ERP task to investigate olfactory functioning in asymptomatic gene carriers.…”

Section: Introductionmentioning

confidence: 99%

Impairments in source memory for olfactory and visual stimuli in preclinical and clinical stages of Huntington's disease

Pirogovsky

Gilbert

Jacobson

et al. 2007

Journal of Clinical and Experimental Neuropsychology

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Individuals in preclinical and clinical stages of Huntington's disease (HD) demonstrate impairments in olfactory functioning. In addition, HD patients are impaired in source memory for verbal stimuli. A task combining both source and odor memory may be particularly sensitive to early changes in HD. The present study examined source and item memory for olfactory and visual stimuli in 10 individuals with HD, 10 asymptomatic HD gene carriers, 8 nongene carriers who had a parent with HD, and 20 normal controls. During the study phase, a male and a female experimenter (sources) presented odors and objects to the participant in an alternating sequence. To assess item memory, a stimulus from the study phase (target) and a novel stimulus (distractor) were presented, and the participant was asked to choose the target. To assess source memory, the experimenter presented a stimulus and asked whether the male or female experimenter had previously presented the stimulus. Results indicate that source memory for both visual and olfactory stimuli was impaired in HD patients compared to normal controls. In asymptomatic gene carriers, however, source memory for olfactory stimuli, but not visual stimuli, was more impaired than in nongene carriers and normal controls. Furthermore, gene carriers and HD patients showed a similar degree of impairment in source memory for olfactory stimuli. The only significant impairment found in item memory was for olfactory stimuli in HD patients. These results suggest that source memory for olfactory stimuli may be particularly sensitive to neuropathological changes in preclinical stages of HD.

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“…Olfactory event-related potentials (OERPs) recorded in relation to olfactory stimulation has demonstrated sensitivity to subtle changes in olfactory functioning associated with aging, disease, and ApoE status [36-45]. OERPs require odor stimulation via specially built olfactometers which control the exact timing of stimulus onset while avoiding simultaneous stimulation of other sensory modalities such as stimulation of the trigeminal system [39,46-49].…”

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confidence: 99%

Individuals at risk for Alzheimer’s disease show differential patterns of ERP brain activation during odor identification

Morgan

Murphy

2012

Behav Brain Funct

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BackgroundStudies suggest that older adults at risk of developing Alzheimer’s disease may show olfactory processing deficits before other signs of dementia appear.MethodsWe studied 60 healthy non-demented individuals, half of whom were positive for the genetic risk factor the Apolipoprotein E ɛ4 allele, in three different age groups. Event-related potentials to visual and olfactory identification tasks were recorded and analyzed for latency and amplitude differences, and plotted via topographical maps.ResultsVarying patterns of brain activation were observed over the post-stimulus epoch for ɛ4- versus ɛ4+ individuals on topographical maps. Individuals with the ɛ4 allele demonstrated different ERP peak latencies during identification of olfactory but not visual stimuli. High correct ApoE classification rates were obtained utilizing the olfactory ERP.ConclusionsOlfactory ERPs demonstrate functional decline in individuals at risk for Alzheimer’s disease at much earlier ages than previously observed, suggesting the potential for pre-clinical detection of AD at very early stages.

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Olfactory and auditory event-related potentials in Huntington's disease.

Cited by 13 publications

References 66 publications

Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease

Functional roles for the striatal-enriched transcription factor, Bcl11b, in the control of striatal gene expression and transcriptional dysregulation in Huntington's disease

Impairments in source memory for olfactory and visual stimuli in preclinical and clinical stages of Huntington's disease

Individuals at risk for Alzheimer’s disease show differential patterns of ERP brain activation during odor identification

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