title: Hyperplasticity in Autism Spectrum Disorder confers protection from Alzheimer's disease.
abstract: Autism Spectrum Disorders (ASD) currently affects approximately 1% of the population causing grave disability and necessitating a better understanding of the currently enigmatic etiology of these disorders. Recent data suggest that some patients with ASD may have a dysfunction in brain plasticity (specifically data from animal models and human studies suggest a propensity toward excessive amount of plasticity). Plasticity is essential to the establishment and maintenance of brain circuitry; however, too much plasticity may lead to instability of structural connections and compromise of functional systems necessary for cognition and behavior. Multiple lines of evidence suggest that plasticity declines throughout the age-span and may underlie age-related cognitive decline. We hypothesize that individuals whose cortex begins as relatively "hyperplastic" (such as may be seen in ASD) should then be relatively protected from age-related cognitive decline (which we suggest is related to a reduction in plasticity). In the current study, we conducted a multiple linear regression using age and diagnosis as predictor variables in order to evaluate strength of the relationship between age, diagnosis or an interaction of the two factors and the degree of modulation in cortical excitability by transcranial magnetic stimulation as an index of cortical plasticity. Results indicate that across the age-span individuals with ASD show a consistently increased modulation of cortical excitability as compared to typically developing individuals, such that the general slope of decline across the age span is matched across both groups. We have argued that an individual's risk of age-related cognitive decline (and risk for manifesting symptoms of dementia) depends on the individual's starting point and slopes of change in plasticity efficiency over the lifespan. Therefore, our results suggest that individuals with ASD might be relatively protected from age-related cognitive decline and the risk of dementia.
authors.affiliation: Berenson-Allen Center for Noninvasive Brain Stimulation, Division of Brain Stimulation and Cognitive Training, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, United States.
authors.forename: Lindsay M
authors.initials: LM
authors.lastname: Oberman
authors.affiliation: Berenson-Allen Center for Noninvasive Brain Stimulation, Division of Brain Stimulation and Cognitive Training, Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, United States. Electronic address: apleone@bidmc.harvard.edu.
authors.forename: Alvaro
authors.initials: A
authors.lastname: Pascual-Leone
mesh_terms: D000293:Adolescent; D000328:Adult; D000375:Aging; D000544:Alzheimer Disease / Q000503:physiopathology* / Q000517:prevention & control; D000067877:Autism Spectrum Disorder / Q000150:complications / Q000503:physiopathology*; D001921:Brain / Q000502:physiology; D016022:Case-Control Studies; D003071:Cognition; D003072:Cognition Disorders / Q000503:physiopathology; D015331:Cohort Studies; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009473:Neuronal Plasticity / Q000502:physiology*; D010641:Phenotype; D012044:Regression Analysis; D050781:Transcranial Magnetic Stimulation; D055815:Young Adult