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NEUROLOGY 2006;67:1011-1017
© 2006 American Academy of Neurology

Brain mechanisms of successful compensation during learning in Alzheimer disease

R. L. Gould, PhD, B. Arroyo, R. G. Brown, PhD, A. M. Owen, PhD, E. T. Bullmore, PhD and R. J. Howard, MD

From the MRC Centre for Neurodegeneration Research (R.L.G., R.J.H.), King’s College London, Institute of Psychiatry, Section of Old Age Psychiatry, London, UK; The Maudsley Hospital (B.A.), London, UK; King’s College London (R.G.B.), Institute of Psychiatry, Department of Psychology, London, UK; MRC Cognition and Brain Sciences Unit (A.M.O.), Cambridge; and Department of Psychiatry (E.T.B.), University of Cambridge, Cambridge, UK.

Address correspondence and reprint requests to Dr. Rebecca Gould, Section of Old Age Psychiatry (P070), Institute of Psychiatry, De Crespigny Park, London, SE5 8AF, UK; e-mail: r.gould{at}iop.kcl.ac.uk

Objective: To determine whether patients with Alzheimer disease (AD) compensate for neuropathologic changes when performing a mnemonic task by recruiting 1) the same brain regions as age-matched, healthy controls, but to a greater extent; 2) additional brain regions not activated by controls; or 3) both.

Methods: Twelve patients with mild probable AD and 12 healthy age- and education-matched controls participated in an fMRI study of successful encoding and retrieval of visuospatial paired associates. To ensure successful performance in both groups, participants were given multiple attempts to learn associations between two and three object locations.

Results: The pattern of brain activity in patients with AD performing an easy version of the task was indistinguishable from that of controls performing a harder version of the task. Increased activation in left medial and right lateral prefrontal cortices was found in patients with AD compared to controls during encoding of two object locations, but not when this level of encoding in patients was compared with encoding of three object locations in controls.

Conclusions: There was no evidence of neural plasticity in the form of recruitment of novel brain regions in patients with Alzheimer disease. Data supported greater recruitment of the same brain regions as age-matched controls as a means of compensating for neuropathology and associated cognitive impairment in Alzheimer disease.

Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the September 26 issue to find the title link for this article.

Supported by the Wellcome Trust.

Disclosure: The authors report no conflicts of interest.

Received June 24, 2005. Accepted in final form May 10, 2006.






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