Affiliations:
Departments of Neurology and Psychiatry & Biobehavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles, and Neurology Service, Neurobehavior Unit, U.S. Department of Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA
Correspondence:
[*]
Correspondence to: Mario F. Mendez, MD, PhD, Neurobehavior Unit, V.A. Greater Los Angeles Healthcare Center, 11301 Wilshire Blvd., Los Angeles, CA 90073, USA. Tel.: +1 310 478 3711/Ext. 42696; Fax: +1 310 268 4181; E-mail: mmendez@UCLA.edu.
Abstract: Alzheimer’s disease (AD) is an age-related neurocognitive disorder that is epidemic in the elderly population. Currently, there are limited pharmacological interventions, and this has heightened the urgency to identify potential preventable or modifiable risk factors that promote resilience to the neuropathological effects of AD. The regular use of two or more languages is one such factor that may increases cognitive reserve through the long-standing executive control involved in managing multiple languages in the brain. There is also evidence that bilingualism is associated with increased brain reserve or maintenance, particularly in frontal-executive structures and networks. This review examines the current, sometimes conflicting literature on bi/multilingualism and AD. These studies have confounding variations in the assessment of age of second language onset, language proficiency, language usage, and whether determining incidence of AD or age of symptom onset. Despite these limitations, most publications support the presence of increased frontal-executive reserve that compensates for the development of AD neuropathology and, thereby, delays the emergence of clinical symptoms of dementia by about 4-5 years. Although regularly speaking more than one language does not protect against AD neuropathology, the delay in its clinical expression has a potentially significant impact on the lifelong morbidity from this age-related disease. Learning other languages may be an important modifiable factor for delaying the clinical expression of AD in later life.
