Farhana Islam1, Benoit H Mulsant2,3, Aristotle N Voineskos2,3, Tarek K Rajji4,5. 1. Human Biology Department, University of Toronto, 300 Huron Street, Toronto, ON, M5S 3J6, Canada. 2. Division of Geriatric Psychiatry, Department of Psychiatry, University of Toronto, Toronto, ON, Canada. 3. Division of Geriatric Psychiatry, Centre for Addiction and Mental Health, 80 Workman Way, 6th floor, Room 6312, Toronto, ON, M6J1H4, Canada. 4. Division of Geriatric Psychiatry, Department of Psychiatry, University of Toronto, Toronto, ON, Canada. tarek.rajji@camh.ca. 5. Division of Geriatric Psychiatry, Centre for Addiction and Mental Health, 80 Workman Way, 6th floor, Room 6312, Toronto, ON, M6J1H4, Canada. tarek.rajji@camh.ca.
Abstract
PURPOSE OF REVIEW: Schizophrenia has been hypothesized to be a syndrome of accelerated aging. Brain plasticity is vulnerable to the normal aging process and affected in schizophrenia: brain-derived neurotrophic factor (BDNF) is an important neuroplasticity molecule. The present review explores the accelerated aging hypothesis of schizophrenia by comparing changes in BDNF expression in schizophrenia with aging-associated changes. RECENT FINDINGS: Individuals with schizophrenia show patterns of increased overall mortality, metabolic abnormalities, and cognitive decline normally observed later in life in the healthy population. An overall decrease is observed in BDNF expression in schizophrenia compared to healthy controls and in older individuals compared to a younger cohort. There is a marked decrease in BDNF levels in the frontal regions and in the periphery among older individuals and those with schizophrenia; however, data for BDNF expression in the occipital, parietal, and temporal cortices and the hippocampus is inconclusive. Accelerated aging hypothesis is supported based on frontal regions and peripheral studies; however, further studies are needed in other brain regions.
PURPOSE OF REVIEW: Schizophrenia has been hypothesized to be a syndrome of accelerated aging. Brain plasticity is vulnerable to the normal aging process and affected in schizophrenia: brain-derived neurotrophic factor (BDNF) is an important neuroplasticity molecule. The present review explores the accelerated aging hypothesis of schizophrenia by comparing changes in BDNF expression in schizophrenia with aging-associated changes. RECENT FINDINGS: Individuals with schizophrenia show patterns of increased overall mortality, metabolic abnormalities, and cognitive decline normally observed later in life in the healthy population. An overall decrease is observed in BDNF expression in schizophrenia compared to healthy controls and in older individuals compared to a younger cohort. There is a marked decrease in BDNF levels in the frontal regions and in the periphery among older individuals and those with schizophrenia; however, data for BDNF expression in the occipital, parietal, and temporal cortices and the hippocampus is inconclusive. Accelerated aging hypothesis is supported based on frontal regions and peripheral studies; however, further studies are needed in other brain regions.
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