Neurochemical basis of the change in attention control and memory encoding in normal aging


Grant Data
Project Title
Neurochemical basis of the change in attention control and memory encoding in normal aging
Principal Investigator
Dr Mak, Henry Ka Fung   (Principal Investigator (PI))
Co-Investigator(s)
Dr Chiu Pui Wai   (Co-Investigator)
Professor Yau Kelvin Kai wing   (Co-Investigator)
Professor Chu Leung Wing   (Co-Investigator)
Dr Kwan Joseph Shiu Kwong   (Co-Investigator)
Dr Wong Wai Ho Savio   (Co-Investigator)
Dr Shea Yat Fung   (Co-Investigator)
Dr Song You-qiang   (Co-Investigator)
Duration
24
Start Date
2015-12-01
Amount
417221
Conference Title
Neurochemical basis of the change in attention control and memory encoding in normal aging
Presentation Title
Keywords
cognitive processes, glutamate, normal aging, proton MR spectroscopy, task-based BOLD-fMRI
Discipline
Imaging
Panel
Biology and Medicine (M)
HKU Project Code
17108315
Grant Type
General Research Fund (GRF)
Funding Year
2015
Status
Completed
Objectives
1 To investigate the relationship between absolute concentrations of Glu, NAA, and other metabolites in the ACC and bilateral hippocampi with activations in BOLD-fMRI during attention and memory-encoding tasks across age groups. Impact: provides a neurochemical basis for the ""compensation hypothesis"" seen in previous fMRI studies; improve understanding of metabolic changes in normal aging. 2 To investigate the possible differences in metabolite concentration and fMRI activation in subjects with high risk of developing AD (APOE-ɛ4 positive) compared to those with low risk. Impact: if metabolic and functional changes are observed in pre-symptomatic subjects with high risk of developing AD, this technique may become a useful tool for non-invasive early diagnosis. 3 To investigate the change in Glu:Gln ratios with age in the ACC and bilateral hippocampi. Impact: close regulation of the breakdown from Glu into Gln could be a protective function against excitotoxicity from excess Glu in the synaptic cleft. Damage to this regulatory mechanism could lead to neuronal death and pathogenesis.