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Neurobiol Aging. 2016 Apr;40:173-180. doi: 10.1016/j.neurobiolaging.2016.01.133. Epub 2016 Feb 22.

β-amyloid, hippocampal atrophy and their relation to longitudinal brain change in cognitively normal individuals.

Author information

1
Department of Neurology, University of California at Davis, Davis, CA, USA. Electronic address: evanfletcher@gmail.com.
2
Douglas Mental Health University Institute, McGill University, Montreal, Canada.
3
Department of Neurology, University of California at Davis, Davis, CA, USA.
4
Division of Biostatistics, School of Medicine, University of California at Davis, Davis, CA, USA.
5
Helen Wills Neuroscience Institute, University of California, Berkeley, Berkeley CA, USA.

Abstract

Recent literature has examined baseline hippocampal volume and extent of brain amyloidosis to test potential synergistic effects on worsening cognition and extent of brain atrophy. Use of hippocampal volume in prior studies was based on the notion that limbic circuit degeneration is an early manifestation of the Alzheimer's Disease (AD) pathophysiology. To clarify these interactions early in the AD process, we tested the effects of amyloid and baseline normalized hippocampal volume on longitudinal brain atrophy rates in a group of cognitively normal individuals. Results showed that the combination of elevated β-amyloid and baseline hippocampal atrophy is associated with increased rates specific to the limbic circuit and splenium. Importantly, this atrophy pattern emerged from a voxelwise analysis, corroborated by regression models over region of interests in native space. The results are broadly consistent with previous studies of the effects of amyloid and baseline hippocampal atrophy in normals, while pointing to accelerated atrophy of AD-vulnerable regions detectable at the preclinical stage.

KEYWORDS:

Alzheimer's; Atrophy; Longitudinal; Neurodegeneration; Normals; β-amyloid

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