Abstract
Amnestic mild cognitive impairment (aMCI) is believed to represent a transitional stage between normal healthy ageing and the development of dementia. In particular, aMCI patients have been shown to have higher annual transition rates to Alzheimer's Disease (AD) than individuals without cognitive impairment. Despite intensifying interest investigating the neuroanatomical basis of this transition, there remain a number of questions regarding the pathophysiological process underlying aMCI itself. A number of recent studies in aMCI have shown specific impairments in connectivity within the default mode network (DMN), which is a group of regions strongly related to episodic memory capacities. However to date, no study has investigated the integrity of the DMN between patients with aMCI and those with a non-amnestic pattern of MCI (naMCI), who have cognitive impairment, but intact memory storage systems. In this study, we contrasted the DMN connectivity in 24 aMCI and 33 naMCI patients using seed-based resting state fMRI. The two groups showed no statistical difference in their DMN intra-connectivity. However when connectivity was analysed according to performance on measures of episodic memory retrieval, the two groups were separable, with aMCI patients demonstrating impaired functional connectivity between the hippocampal formation and the posterior cingulate cortex. We provide evidence that this lack of connectivity is driven by impaired communication from the posterior cingulate hub and does not simply represent hippocampal atrophy, suggesting that posterior cingulate degeneration is the driving force behind impaired DMN connectivity in aMCI.
Highlights
Introduction common pathophysiological mechanism withAlzheimer’s Disease (AD) (Dubois and Albert, 2004)
When assessing the relationship between RAVLT7/5 scores and default mode network (DMN) connectivity in the cohort of patients with Amnestic mild cognitive impairment (aMCI), poor episodic memory retrieval was related to impairments in connectivity strength between the posterior cingulate cortex (PCC)–hippocampal formation (HF) (r= 0.552, p< 0.005), retrosplenial cortex (RSp)–HF (r= 0.498, p< 0.05), temporoparietal junction (TPJ)–ventromedial prefrontal cortex (vMPFC) (r= 0.448, p< 0.05), PCC–lateral temporal cortex (LTC) (r= 0.437, p< 0.05) and RSp–PHC (r= 0.429, p< 0.05)
In non-amnestic pattern of Mild cognitive impairment (MCI) (naMCI) patients, significant correlations were found between the dorsomedial prefrontal cortex (dMPFC)–posterior intra-parietal lobule (pIPL) (r= 0.502, r< 0.005), PCC–LTC (r= 0.370, p< 0.05), and TPJ–HF (r= –0.429, p< 0.05)
Summary
Introduction common pathophysiological mechanism withAD (Dubois and Albert, 2004). In contrast, non-amnestic (naMCI) patients have preservedMild cognitive impairment (MCI) is a clinical state of cognitive episodic memory and as such are more likely to transition to other decline “greater than expected for an individual’s age and education forms of dementia (Petersen et al, 2009). In regard to neurobiological level” (Gauthier et al, 2006) and has been proposed to represent an markers, patients with aMCI have decreased grey matter volume in intermediate stage between normal ageing and dementia (Petersen the hippocampus (Shi et al, 2009) along with impairments in hipet al., 2009). The annual rate of progression from MCI to Alzheimer’s pocampus connectivity whilst completing memory tasks (Bai et al., Disease (AD) is approximately 14%, which is markedly greater than 2009). These differences have been localised to the left the expected 1–2% annual incidence of AD (Petersen et al, 2009). Hippocampus (Lye et al, 2006), with decreased grey matter volume
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