Abstract Details

Title Prosodic Impairment as a Marker of apoE4 Status in logopenic variant Primary Progressive Aphasia with AD Pathology

Topic Aging, Dementia, and Behavioral Neurology

Presentation(s) P2 - Poster Session 2 (5:30 PM-6:30 PM)

Poster/Presentation
Number 9-032

Objective

To explore the effects of underlying Alzheimer’s disease (AD) pathology on impaired prosody in patients with logopenic variant Primary Progressive Aphasia (lvPPA).

Background

We previously reported on a limited range of fundamental frequency (f0, the physical property of sound typically used to represent perceived pitch) in a group of non-aphasic patients with behavioral variant Frontotemporal Degeneration (FTD). More recently we demonstrated a similar finding in nonfluent-agrammatic PPA, and associated it with cerebrospinal fluid (CSF) levels of phosphorylated tau (pTau). Patients with semantic variant PPA showed no impairment in their prosodic range, while patients with logopenic variant PPA (lvPPA) exhibited an intermediate impairment. We hypothesized worsening of prosodic range in lvPPA carrying apolipoprotein E e4 (apoE4) genotype.

Design/Methods We automatically segmented and analyzed digitized semi-structured speech samples from 29 patients with lvPPA with a mildly reduced f0 range (mean 5.0±1.87 semitones). Within this group we compared f0 range in carriers of apoE4 (n=9, 44% males, mean age 68±10y, mean disease duration 4±2y, mean MMSE 24) to that of noncarriers (n=15, 26% males, mean age 65±7y, mean disease duration 3.5±1.5y, mean MMSE 20), covarying for these demographic characteristics. In a subset of patients who had CSF within 6 months of audio collection (n=22) we ran linear regression models associating f0 range, sex and age as predictors of Abeta42 levels.

Results

There was a significant limitation of f0 range in lvPPA patients who are carriers of apoE4 (mean 4.63±0.9 ST) compared to non-carriers (5.42±1.82 ST; p=0.03, with MMSE score and disease duration as significant covariables). The best fit regression model implicated f0 range (coef.=-20.8), male sex (coef.=-76.7) and age (coeff.=6.7) as highly predictive of Abeta42 levels in CSF (R²=0.37, p=0.04).

Conclusions Impaired f0 range is a potential clinical marker for underlying AD pathology associated with apoE4 in patients with an lvPPA phenotype.

Authors/Disclosures
Naomi Nevler, MD (Hospital of the University of Pennsylvania) PRESENTER	No disclosure on file
Sharon Ash (University of Pennsylvania)	No disclosure on file
David Irwin, MD (University of Pennsylvania)	The institution of Dr. Irwin has received research support from NIH. The institution of Dr. Irwin has received research support from Prevail. The institution of Dr. Irwin has received research support from Passage Bio. The institution of Dr. Irwin has received research support from Alector. The institution of Dr. Irwin has received research support from Transposon. The institution of Dr. Irwin has received research support from Denali. The institution of Dr. Irwin has received research support from Cervo Med.
	No disclosure on file
Murray Grossman, MD, FAAN (University of Pennsylvania)	Dr. Grossman has received personal compensation in the range of $5,000-$9,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for Neurology. The institution of Dr. Grossman has received research support from NIH.

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