Poster E46, Saturday, August 18, 3:00 – 4:45 pm, Room 2000AB
Bilingualism delays age of symptom onset in the language variant but not the amnestic variant of Alzheimer’s dementia
Jessica de Leon1, Stephanie Grasso2, Ariane Welch1, Zachary Miller1, Wendy Shwe1, Maya L. Henry2, Maria Luisa Gorno-Tempini1;1University of California, San Francisco, 2University of Texas, Austin
Bilingualism may be a contributor to cognitive reserve and therefore serve as a protective factor against the onset of Alzheimer’s dementia (AD). However, results have been mixed. Whereas some studies have shown up to a 5-year delay in symptom onset for bilingual speakers, others have found no difference in the age of symptom onset between speaker groups (i.e. mono- versus bi-lingual speakers). Historically, AD was viewed as a single diagnostic entity; however, in the past several decades, research has demonstrated that AD comprises a spectrum of distinct clinical variants, including but not limited to, logopenic variant primary progressive aphasia (lvPPA) and amnestic AD. The amnestic variant of AD is characterized by episodic memory deficits and bilateral hippocampal and mesial temporal lobe atrophy. The language variant of AD, lvPPA, is characterized by impaired phonological processing (i.e. impaired repetition and word retrieval), with left temporo-parietal atrophy. Though these two variants share the underlying neuropathology of amyloid-beta plaques and tau tangles, they differ in the primary affected neural network (memory versus language). To date, studies have yet to delineate the effects of bilingualism within different AD variants. Therefore, the aims of this retrospective study were twofold. First, we examined if the proportion of bilingual and monolingual speakers were comparable across clinical variants, in a cohort of well-characterized patients who were diagnosed with either amnestic AD or lvPPA (based on established clinical and imaging criteria). We predicted that our speaker groups would not differ on the basis of clinical diagnosis. Second, we examined the effect of bilingualism on age of symptom onset, with the prediction that bilingual speakers in each clinical variant would show a delay in symptom onset relative to monolingual speakers. We identified 40 bilinguals (24 with amnestic AD and 16 with lvPPA) and 240 monolinguals (184 with amnestic AD and 63 with lvPPA), via chart review. Within clinical variant, the bilingual speakers did not differ from monolingual speakers by sex, years of education, handedness or neuropsychological measures; however, as expected, our groups differed by immigrant status (p <.0001). Results indicated that the proportion of bilingual and monolingual speakers were comparable across the clinical variants. With regard to a potential delay in symptom onset, results indicated a significant, 5-year delay in age of symptom onset for bilingual relative to monolingual speakers with lvPPA (64 for bilinguals, 59 for monolinguals, p = 0.03), but such an effect was not observed in the amnestic AD cohort. Moreover, the effect of bilingualism on age of onset was independent of other cognitive reserve variables (i.e. education, sex, and immigrant status). Contrary to our hypothesis, results from our cohort suggest that bilingualism may serve as a unique cognitive reserve variable in lvPPA, but not in amnestic AD. One possible explanation for this finding may be that bilingualism has distinct effects on the specific neural networks underlying the manifestation of these different clinical variants. Future research should investigate the neural mechanisms by which bilingualism contributes to cognitive reserve for select clinical populations.
Topic Area: Language Disorders