Abstract
BackgroundAlzheimer's disease (AD) is generally thought to spare primary sensory function; however, such interpretations have drawn from a literature that has rarely taken into account the variable cognitive declines seen in patients with AD. As these cognitive domains are now known to modulate cortical somatosensory processing, it remains possible that abnormalities in somatosensory function in patients with AD have been suppressed by neuropsychological variability in previous research.MethodsIn this study, we combine magnetoencephalographic (MEG) brain imaging during a paired-pulse somatosensory gating task with an extensive battery of neuropsychological tests to investigate the influence of cognitive variability on estimated differences in somatosensory function between biomarker-confirmed patients on the AD spectrum and cognitively-normal older adults.FindingsWe show that patients on the AD spectrum exhibit largely non-significant differences in somatosensory function when cognitive variability is not considered (p-value range: .020–.842). However, once attention and processing speed abilities are considered, robust differences in gamma-frequency somatosensory response amplitude (p < .001) and gating (p = .004) emerge, accompanied by significant statistical suppression effects.InterpretationThese findings suggest that patients with AD exhibit insults to functional somatosensory processing in primary sensory cortices, but these effects are masked by variability in cognitive decline across individuals.FundingNational Institutes of Health, USA; Fremont Area Alzheimer's Fund, USA
Highlights
The pathological trajectory of Alzheimer’s disease (AD) is thought to begin as early as 20 years prior to the manifestation of hallmark declines in memory and other cognitive functions, beginning with the accumulation of amyloid-b “plaques” and fibrillary “tangles” rich in hyperphosphorylated tau [1,2]
We found a significant relationship between learning domain scores and amyloid-b SUV ratios (SUVR), such that increased amyloid-b pathology in primary somatosensory cortex predicted worse learning performance (partial correlation; r(33) = .47, p = .005; Fig. 5)
Despite an extensive literature reporting somatosensory dysfunction in animal models of AD [28,29], very little evidence exists supporting such pathology in human patients. While this discrepancy might be partially attributable to inherent differences in the AD neuropathology of humans and that observed in animal models, we find evidence that it might instead stem from a robust suppression effect attributable to between-participant variability in cognitive function in AD, explicitly in two key domains: attention and processing speed
Summary
The pathological trajectory of Alzheimer’s disease (AD) is thought to begin as early as 20 years prior to the manifestation of hallmark declines in memory and other cognitive functions, beginning with the accumulation of amyloid-b “plaques” and fibrillary “tangles” rich in hyperphosphorylated tau [1,2]. Alzheimer’s disease (AD) is generally thought to spare primary sensory function; such interpretations have drawn from a literature that has rarely taken into account the variable cognitive declines seen in patients with AD. As these cognitive domains are known to modulate cortical somatosensory processing, it remains possible that abnormalities in somatosensory function in patients with AD have been suppressed by neuropsychological variability in previous research.
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