SAGE KE Bulletin Board

Comment on Lesné et al. “A specific amyloid-ß protein assembly in the brain impairs memory”

10 April 2006

Dietmar R Thal

Comment on Lesné et al. “A specific amyloid-ß protein assembly in the brain impairs memory�? Nature 449 (2006) 352-357

Lesné et al. (1) report that the 56-kDa soluble amyloid-ß (Aß) assembly causes memory deficits in middle aged Tg2576 mice. Administration of the Aß assembly to young rats leads to memory disruption. After stopping the administration of 56-kDa soluble Aß assemblies rats recovered and showed similar response to memory tasks as untreated animals. The fact that the Aß-assembly-induced alteration of learning in young rats appears to be reversible would mean that Alzheimer’s disease related memory deficits may be reversible when treated adequately. Unfortunately, patients with early Alzheimer’s disease already exhibit substantial neuronal loss in distinct areas of the brain (2). Therefore, one cannot expect restitutio ad integrum when treating AD-patients by reducing or eliminating Aß-oligomeric complexes, such as the 56-kDa soluble Aß assembly, from brain. However, such a treatment may stop further cognitive alterations and, if there is a population of recoverable neurons, may reduce the deficits of the patient.


1. S. Lesne, M. T. Koh, L. Kotilinek, R. Kayed, C. G. Glabe, A. Yang, M. Gallagher, K. H. Ashe, A specific amyloid-beta protein assembly in the brain impairs memory. Nature 440, 352-357 (Mar 16, 2006).

2. T. Gomez-Isla, J. L. Price, D. W. McKeel, Jr., J. C. Morris, J. H. Growdon, B. T. Hyman, Profound loss of layer II entorhinal cortex neurons occurs in very mild Alzheimer's disease. J Neurosci 16, 4491-4500 (Jul 15, 1996).

Science of Aging Knowledge Environment. ISSN 1539-6150