Insulin and the Blood‐Brain Barrier

Banks, William A.; Lim, Wee Shiong

doi:10.1002/9783527611225.ch12

Cited by 2 publications

(2 citation statements)

References 103 publications

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“…Cytokines play a central role in the system by which the peripheral immune system communicates with the CNS (Dilger and Johnson 2008). They may enter the CNS through areas of blood–brain barrier that are highly permeable or through active transport (Banks 2001). Cytokines may also bind to receptors within cerebral blood vessels and induce the production of second messengers that, then, diffuse into the brain (Maier and Watkins 2003).…”

Section: Cns Immune Regulationmentioning

confidence: 99%

The inflammation hypothesis in geriatric depression

Alexopoulos

Morimoto

2011

Int J Geriat Psychiatry

183

109

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Background A large body of research has focused on “mediating mechanisms” and predisposing brain abnormalities to geriatric depression, but little is known about its etiology. This paper examines whether age-related and comorbid disease-related immune deregulation is an etiologic contributor to geriatric depression. Methods This article reviews findings on neuroinflammation during the aging process and depression as well as studies of anti-inflammatory actions of classical antidepressants and antidepressant actions of anti-inflammatory agents. Results Aging results in increased peripheral immune responses, impaired peripheral-CNS immune communication, and a shift of the CNS into a pro-inflammatory state. These exaggerated and prolonged immune responses may lead to changes in the function of emotional and cognitive networks pertinent to geriatric depression and to behavioral changes reminiscent of the depressive and cognitive symptoms of geriatric depression. Some antidepressants may reduce the expression of inflammation markers. Limited data suggest that some anti-inflammatory agents may have antidepressant properties. Conclusions A synthesis of available findings suggests that aging-related and comorbid disease-related inflammatory processes may promote changes in the neural systems predisposing to geriatric depression or facilitating metabolic changes that mediate depressive syndromes. The “inflammation hypothesis” in geriatric depression cannot be tested in its entirety, but it can lead to testable hypotheses and data on mechanisms by which inflammatory processes promote geriatric depression. The significance of such an effort is that it may lead to a novel treatment development model bringing to bear recent advances of anti-inflammatory pharmacology to the treatment of depressed elderly patients.

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Section: Cns Immune Regulationmentioning

confidence: 99%

The inflammation hypothesis in geriatric depression

Alexopoulos

Morimoto

2011

Int J Geriat Psychiatry

183

109

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“…Inflammatory cytokines communicate the immune status of the periphery to the CNS through the following mechanisms: 1. Active transport: Certain cytokines ( IL-1 beta, IL-6, TNFα, and IL 1 alpha) cross the blood brain barrier through a saturable transport system (Banks 2001). 2.…”

Section: Periphery – Brain Immune Communicationmentioning

confidence: 99%

Immunity, Aging, and Geriatric Depression

Morimoto

Alexopoulos

2011

Psychiatric Clinics of North America

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Despite pioneering findings on immune functions in various depressive syndromes, few recent studies focus on the role of inflammation and its potential in generating novel antidepressant therapies. We suggest that geriatric depression is the behavioral syndrome par excellence in which inflammatory processes are likely to play an etiological role. We base this assertion on the following observations: Geriatric depression occurs in the context of medical and neurological illnesses in which inflammatory processes are part of their pathogenesis. Both aging and depression are associated with pronounced and prolonged immune responses. Brain areas related to mood processing, have increased inflammatory responses during aging. Moreover, the connectivity among mood regulating structures may be modulated by inflammatory responses. Geriatric depression exacerbates the pathology of its comorbid medical and neurological disorders raising the question whether depression-related inflammatory changes mediate the worsening of their outcomes. Finally, geriatric depression often occurs in persons exposed to chronic stress, a state precipitating geriatric depression and triggering pro-inflammatory responses. The clinical lesson derived from the available information is that depressed older adults should be examined for inflammatory disorders or risk factors of inflammation. It is premature to use anti-inflammatory agents in the treatment of geriatric depression. However, treatment of co-morbid conditions increasing CNS inflammatory responses can have general health benefits and should be part of clinical practice. Neuroimaging may identify microstructural abnormalities and dysfunction of neural networks associated with inflammatory processes accompanying geriatric depression. Transgenic animal models may help to identify candidate anti-inflammatory agents that later may be tested in clinical trials of geriatric depression.

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Insulin and the Blood‐Brain Barrier

Cited by 2 publications

References 103 publications

The inflammation hypothesis in geriatric depression

The inflammation hypothesis in geriatric depression

Immunity, Aging, and Geriatric Depression

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