Lower hippocampal volume not related to AD pathology in late-life depression
Lower hippocampal volume is not associated with amyloid pathology, negating the common belief that changes in hippocampal volume in late-life depression are due to prodromal Alzheimer’s disease, according to a recent study.
To investigate the association between lower hippocampal volume in late-life depression and Alzheimer’s disease pathology, a prospective study was conducted involving 100 participants (48 currently depressed older adults and 52 age- and gender-matched healthy comparison participants who underwent structural MRI, flutemetamol (18F) amyloid positron emission tomography imaging, apolipoprotein E genotyping, and neuropsychological assessment).
Hippocampal volumes were manually defined and normalized for total intracranial volume. Researchers quantified amyloid binding using the standardized uptake value ratio in one cortical composite volume of interest. They examined group differences in hippocampal volume, group differences in amyloid uptake and in the proportion of positive amyloid scans, and the association between hippocampal volume and cortical amyloid uptake.
There was a significant difference in mean normalized total hippocampal volume between patients and comparison participants. However, no between-group differences were observed in cortical amyloid uptake or proportion of amyloid-positive participants.
There remained a significant difference in hippocampal volume even after the amyloid-positive participants were excluded. No association existed between hippocampal volume and amyloid uptake in either patients or comparison participants.
“Hippocampal volume is commonly decreased in late-life depression,” researchers said. “According to the depression-as-late-life-neuropsychiatric-disorder model, lower hippocampal volume in late-life depression is associated with neurodegenerative changes.”
A separate study found an association between depression and cognitive impairment. The mechanisms by which depression could induce cognitive impairment were hippocampal atrophy, alterations in glucocorticoid secretion, cerebrovascular compromise, deposition of β-amyloid plaques, chronic inflammation, apolipoprotein E status and deficits of nerve growth factors. [Focus 2017;15:35-41]