Alzheimer Disease: Haaland KY

Buxbaum LJ, Haaland KY, Hallett M, Wheaton L, Heilman KM, Rodriguez A, Gonzalez Rothi LJ. · Moss Rehabilitation Research Institute, Philadelphia, Pennsylvania 19141, USA. · Am J Phys Med Rehabil. · Pubmed #18209511 No free full text.

Abstract: Limb apraxia is a common disorder of skilled, purposive movement that is frequently associated with stroke and degenerative diseases such as Alzheimer disease. Despite evidence that several types of limb apraxia significantly impact functional abilities, surprisingly few studies have focused on development of treatment paradigms. Additionally, although the most disabling types of apraxia reflect damage to gesture and/or object memory systems, existing treatments have not fully taken advantage of principles of experience known to affect learning and neural plasticity. We review the current state of the art in the rehabilitation of limb apraxia, indicate possible points of contact with the learning literature, and generate suggestions for how translational principles might be applied to the development of future research on treatment of this disabling disorder.

Stricker NH, Schweinsburg BC, Delano-Wood L, Wierenga CE, Bangen KJ, Haaland KY, Frank LR, Salmon DP, Bondi MW. · New Mexico VA Healthcare System, USA. · Neuroimage. · Pubmed #19100839 No free full text.

Abstract: The retrogenesis model of Alzheimer's disease (AD) posits that white matter (WM) degeneration follows a pattern that is the reverse of myelogenesis. Using diffusion tensor imaging (DTI) to test this model, we predicted greater loss of microstructural integrity in late-myelinating WM fiber pathways in AD patients than in healthy older adults, whereas differences in early-myelinating WM fiber pathways were not expected. We compared 16 AD patients and 14 demographically-matched healthy older adults with a whole-brain approach via tract-based spatial statistics (TBSS), and a region of interest (ROI) approach targeting early-myelinating (posterior limb of internal capsule, cerebral peduncles) and late-myelinating (inferior longitudinal fasciculus [ILF], superior longitudinal fasciculus [SLF]) fiber pathways. Permutation-based voxelwise analysis supported the retrogenesis model. There was significantly lower fractional anisotropy (FA) in AD patients compared to healthy older adults in late-myelinating but not early-myelinating pathways. These group differences appeared to be driven by loss of myelin integrity based on our finding of greater radial diffusion in AD than in healthy elderly. ROI analyses were generally in agreement with whole-brain findings, with significantly lower FA and increased radial diffusion in the ILF in the AD group. Consistent with the retrogenesis model, AD patients showed demonstrable changes in late-myelinating WM fiber pathways. Given greater change in the ILF than the SLF, wallerian degeneration secondary to cortical atrophy may also be a contributing mechanism. Knowledge of the pattern of WM microstructural changes in AD and its underlying mechanisms may contribute to earlier detection and intervention in at-risk groups.