P300 Energy Loss in Aging and Alzheimer's Disease

Issue title: Imaging the Alzheimer Brain

Guest editors: J. Wesson Ashford, Allyson Rosen, Maheen Adamson, Peter Bayley, Osama Sabri, Ansgar Furst, Sandra E. Black and Michael Weiner

Article type: Research Article

Authors: Ashford, J. Wesson^{a; e; *} | Coburn, Kerry L.^b | Rose, Terrence L.^c | Bayley, Peter J.^{d; e}

Affiliations: [a] War Related Illness and Injury Study Center, VA Palo Alto Health Care System, Palo Alto, CA, USA | [b] Department of Psychiatry and Behavioral Sciences, Mercer University School of Medicine, GA, USA | [c] Multivariate Measurement Technology Corporation, Sherman, CT, USA | [d] VA Palo Alto Health Care System, Palo Alto, CA, USA | [e] Department of Psychiatry and Behavioral Sciences, Stanford University, Palo Alto, CA, USA

Correspondence: [*] Correspondence to: J. Wesson Ashford M.D., Ph.D., VA Palo Alto Health Care System, 3801 Miranda Avenue, Mailcode 151Y, Palo Alto, CA 94304-1290, USA. Tel.: +650 852 3287; Fax: +650 852 3297; E-mail: ashford@stanford.edu.

Abstract: The amplitude of the event-related potential P300 component is sensitive to aging and Alzheimer's disease (AD). Using a standard 20-electrode configuration, the P300 was measured during an “oddball” task in 14 young normal individuals (YN: 21–41 years), 11 elderly normal individuals (EN: 61–80 years), and 23 probable AD patients (AD: 63–93 years; NINCDS-ADRDA criteria). P300 latencies and amplitudes were measured at PZ. Additionally, algorithmic calculations were made from spline plots across the 11 central electrodes for P300 peak voltage latency and total field energy. The measured versus calculated latencies were in general agreement. Furthermore, the measured P300 voltage amplitude was closely related to the calculated total field energy. P300 voltage latency was significantly prolonged in the elderly, but not more so in AD patients (average latency [ms ± SD]; YN, 315 ± 21; EN, 364 ± 48 and AD, 361 ± 56). P300 amplitude showed the expected pattern of change from young to elderly to AD (average voltage [uV ± SD]; YN, 13 ± 5.1; EN, 8.3 ± 2.8; and AD, 4.9 ± 3.3). Summing the squares of each wave (an indication of power: P = V2 R) showed the expected change with age more strongly than the P300 amplitude (average ± SD; YN, 44,397 ± 32,386; EN, 9,996 ± 7,018; and AD, 3,347 ± 2,971). Mini-Mental State Exam scores showed no relationship to P300 latency and minimal relationship to amplitude. Results suggest that the P300 is not obliterated in early AD, but is barely discernable in late AD. The approaches to calculating the P300 described here are potentially useful for measuring specific neural systems affected by aging and AD.

Keywords: Aging, Alzheimer's disease, dementia, event-related potentials, P300, P3a, P3b

DOI: 10.3233/JAD-2011-0061

Journal: Journal of Alzheimer's Disease, vol. 26, no. s3, pp. 229-238, 2011