A core avenue for transcultural research on dementia: on the cross-linguistic generalization of language-related effects in Alzheimer‘s disease and Parkinson’s disease

 International Journal of Geriatric Psychiatry

Calvo, N., Ibáñez, A., Muñoz, E., & García, A. M. (2017). A core avenue for transcultural research on dementia: On the crosslinguistic generalization of language-related effects in Alzheimer’s and Parkinson’s disease. International Journal of Geriatric Psychiatry 33(6), 814-823 Online: http://bit.ly/2nj7yyo.

Si bien el lenguaje es una fuente crítica de variabilidad intercultural, este tema no ha sido abordado en dos líneas de investigación crecientes sobre la relación entre lenguaje y demencias. Este trabajo busca abrir dicho ámbito indagación, apuntando las limitaciones de la evidencia sobre (i) los efectos neuroprotectores del bilingüismo en la enfermedad de Alzheimer y (ii) déficits específicos a nivel semántico como marcadores de la enfermedad de Parkinson. Además, se identifican nuevas líneas de estudio para propiciar el desarrollo de este campo.

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A core avenue for transcultural research on dementia: on the cross-linguistic generalization of language-related effects in Alzheimer‘s disease and Parkinson’s disease

 International Journal of Geriatric Psychiatry

Calvo, N., Ibáñez, A., Muñoz, E., & García, A. M. (2017). A core avenue for transcultural research on dementia: On the crosslinguistic generalization of language-related effects in Alzheimer’s and Parkinson’s disease. International Journal of Geriatric Psychiatry 33(6), 814-823 Online: http://bit.ly/2nj7yyo.

Language is a key source of cross-cultural variability, which may have both subtle and major effects on neurocognition. However, this issue has been largely overlooked in two flourishing lines of research assessing the relationship between language-related neural systems and dementia. This paper assesses the limitations of the evidence on (i) the neuroprotective effects of bilingualism in Alzheimer’s disease and (ii) specific language deficits as markers of Parkinson’s disease.

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