Physical Activity and Brain Plasticity in Late Adulthood.

Physical activity and brain plasticity in late adulthood.

Dialogues Clin Neurosci. 2013 Mar; 15(1): 99-108
Erickson KI, Gildengers AG, Butters MA

The human brain shrinks with advancing age, but recent research suggests that it is also capable of remarkable plasticity, even in late life. In this review we summarize the research linking greater amounts of physical activity to less cortical atrophy, better brain function, and enhanced cognitive function, and argue that physical activity takes advantage of the brain’s natural capacity for plasticity. Further, although the effects of physical activity on the brain are relatively widespread, there is also some specificity, such that prefrontal and hippocampal areas appear to be more influenced than other areas of the brain. The specificity of these effects, we argue, provides a biological basis for understanding the capacity for physical activity to influence neurocognitive and neuropsychiatric disorders such as depression. We conclude that physical activity is a promising intervention that can influence the endogenous pharmacology of the brain to enhance cognitive and emotional function in late adulthood. HubMed – depression

Applications of transcranial magnetic stimulation and magnetic seizure therapy in the study and treatment of disorders related to cerebral aging.

Dialogues Clin Neurosci. 2013 Mar; 15(1): 87-98
Luber B, McClintock SM, Lisanby SH

Transcranial magnetic stimulation (TMS) can be used to probe cortical function and treat neuropsychiatric illnesses. TMS has demonstrated neuroplastic effects akin to long-term potentiation and long-term depression, and therapeutic applications are in development for post-stroke recovery, Alzheimer’s disease, and depression in seniors. Here, we discuss two new directions of TMS research relevant to cerebral aging and cognition. First, we introduce a paradigm for enhancing cognitive reserve, based on our research in sleep deprivation. Second, we discuss the use of magnetic seizure therapy (MST) to spare cognitive functions relative to conventional electroconvulsive therapy, and as a means of providing a more potent antidepressant treatment when subconvulsive TMS has shown modest efficacy in seniors. Whether in the enhancement of cognition as a treatment goal, or in the reduction of amnesia as a side effect, these approaches to the use of TMS and MST merit further exploration regarding their clinical potential. HubMed – depression

Chronic depression as a model disease for cerebral aging.

Dialogues Clin Neurosci. 2013 Mar; 15(1): 77-85
Bewernick BH, Schlaepfer TE

Conceptualizations of the underlying neurobiology of major depression have changed their focus from dysfunctions of neurotransmission to dysfunctions of neurogenesis and neuroprotection. The “neurogenesis hypothesis of depression” posits that changes in the rate of neurogenesis are the underlying mechanism in the pathology and treatment of major depression. Stress, neuroinflammation, dysfunctional insulin regulation, oxidative stress, and alterations in neurotrophic factors possibly contribute to the development of depression. The influence of antidepressant therapies, namely pharmacotherapy and neuroprotectants, on cellular plasticity are summarized. A dysfunction of complex neuronal networks as a consequence of neural degeneration in neuropsychiatric diseases has led to the application of deep brain stimulation. We discuss the way depression seen in the light of the neurogenesis hypothesis can be used as a model disease for cerebral aging. A common pathological mechanism in depression and cerebral aging-a dysfunction of neuroprotection and neurogenesis-is discussed. This has implications for new treatment methods. HubMed – depression