Ging-Yuek Robin Hsiung

Our study investigates whether neural activity corroborates existing behavioral evidence that familiar music is beneficial to Alzheimer’s Disease (AD) patients in music therapy (MT). We hypothesized that AD patients will show different patterns of blood-oxygen-level dependent (BOLD) activity, compared to healthy elderly controls, when listening to familiar versus unfamiliar music. Ten subjects with mild to moderate AD and ten healthy elderly controls underwent functional magnetic resonance imaging (fMRI) while listening to blocks of differing auditory stimuli, interleaved with blocks of static noise. The stimuli were a) familiar music b) unfamiliar music c) scrambled familiar music d) scrambled unfamiliar music. Each subject was exposed to each stimulus category twice, in randomized order. We found different patterns of activation emerge for AD patients versus control subjects when listening to familiar music and when listening to unfamiliar music. For familiar music, AD patients had more activated areas than control subjects. For unfamiliar music, control subjects had more activated areas than AD subjects. However, only one investigated area was significantly differently activated between the 2 groups. This area was the temporopolar area, and it was significantly more active in controls than in AD subjects during unfamiliar music. In this paper, we will first discuss the known neurological substrates of music processing and then the possible functions of the areas found significantly active in response to our musical stimuli. We begin with providing background information on music and the brain.

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Objective: This thesis aimed to investigate cortical thickness in presymptomatic GRNand C9ORF72 mutation carriers prior to the onset of frontotemporal dementia (FTD).Methods: Subjects were recruited from 16 families with a family history of FTD causedby GRN or C9ORF72 mutations. The C9ORF72 group consisted of 8 mutation carriers(age 50.25 ± 6.90 years), 11 non-carrier family member controls (age 52.82 ± 17.15years), and 3 affected carriers (age 55.00 ± 1.00 years). The GRN group consisted of 6mutation carriers (age 53.33 ± 9.67 years) and 9 non-carrier family member controls(age 52.11 ± 8.82). Between group differences in cortical thickness were assessedusing a surface based vertex-by-vertex model correcting for age, sex, MMSE and yearsto mean age of family onset. Significant clusters are reported at 10mm, 15mm and20mm of smoothing and those identified at all three, two consecutive or one smoothinglevel are reported with strong, moderate and weak confidence, respectively.Results: Compared to non-carrier control family members, the C9ORF72 mutationcarriers exhibited no difference in cognitive domain scores, but presented with strong tomoderate asymmetrical patterns of thinning in the right temporoinsular and leftmediofrontal and temporal regions. Compared to non-carrier controls, the GRN mutationcarriers exhibited decreased performance on domains of working memory (p = 0.02)and executive function (p = 0.01), with a trend towards reduced language (p = 0.06) andvisuospatial (p = 0.08) domains, but did not exhibit any difference in cortical thicknesswhen compared to the non-carrier control family members.Conclusions: With the use of genetic screening and neuroimaging analyses this thesisdemonstrated that grey matter atrophy occurs prior to cognitive decline in C9ORF72mutation carriers, while GRN carriers exhibit subtle changes in cognitive domains priorto cortical grey matter atrophy. These findings could prove to be highly valuable as theysuggest that the mechanism of disease progression between the two mutations maydiffer. As such, each mutation may require specific neuroimaging methods to trackmorphological changes prior to cognitive decline and clinical onset.

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