Immunity and cognition: what do age-related dementia, HIV-dementia and ‘chemo-brain’ have in common?

Kipnis, Jonathan; Derecki, Noel; Yang, Chunhui; Scrable, Heidi

doi:10.1016/j.it.2008.07.007

Cited by 76 publications

(51 citation statements)

References 81 publications

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“…A growing body of research has established that in certain contexts T cells act together with glial cells to promote neuroprotection and survival [8-13]. Although it has long been known that during pathogenic conditions (e.g., multiple sclerosis, brain infection), the presence of T cells in the CNS is associated with an increased risk of neuronal damage [14,15].…”

Section: The Neuroprotective Effects Of Cellular Immunitymentioning

confidence: 99%

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging

Petitto¹

2014

J Neurol Disord

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Emerging evidence indicates that neuroimmunological changes in the brain can modify intrinsic brain processes that are involved in regulating neuroplasticity. Increasing evidence suggests that in some forms of motor neuron injury, many neurons do not die, but reside in an atrophic state for an extended period of time. In mice, facial motor neurons in the brain undergo a protracted period of degeneration or atrophy following resection of their peripheral axons. Reinjuring the proximal nerve stump of the chronically resected facial nerve stimulates a robust reversal of motor neuron atrophy which results in marked increases in both the number and size of injured motor neurons in the facial motor nucleus. In this brief review, we describe research from our lab which indicates that the reversal of atrophy in this injury model is dependent on normal cellular immunity. The role of T cells in this unique form of neuroplasticity following injury and in brain aging, are discussed. The potential role of yet undiscover intrinsic actions of recombination activating genes in the brain are considered. Further research using the facial nerve reinjury model could identify molecular signals involved in neuroplasticity, and lead to new ways to stimulate neuroregenerative processes in neurotrauma and other forms of brain insult and disease.

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Section: The Neuroprotective Effects Of Cellular Immunitymentioning

confidence: 99%

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging

Petitto¹

2014

J Neurol Disord

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“…However, other cellular immune factors are also found to be involved in neuroplastic processes and related neurocognitive functions, i.e., memory and learning (Kipnis et al 2008;Martino et al 2011;Ron-Harel et al 2011). These cellular factors include CD4?…”

Section: Neuroimmunomodulation In Depression: An Emerging Conceptmentioning

confidence: 99%

“…Further, evidence suggests a role for humoral and cellular immune factors mediating anti-neuroplastic processes and higher neurocognitive functions in depression-like behaviour (i.e. cognitive dysfunction and sickness-like behaviour) (Kipnis et al 2008;McAfoose and Baune 2009;Eyre and Baune 2012a, b).…”

Section: Introductionmentioning

confidence: 99%

Neuroimmunomodulation in unipolar depression: a focus on chronobiology and chronotherapeutics

Eyre

Baune

2012

J Neural Transm

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The rising burden of unipolar depression along with its often related sleep disturbances, as well as increasing rates of sleep restriction in modern society, make the search for an extended understanding of the aetiology and pathophysiology of depression necessary. Accumulating evidence suggests an important role for the immune system in mediating disrupted neurobiological and chronobiological processes in depression. This review aims to provide an overview of the neuroimmunomodulatory processes involved with depression and antidepressant treatments with a special focus on chronobiology, chronotherapeutics and the emerging field of immune-circadian bi-directional crosstalk. Increasing evidence suggests that chronobiological disruption can mediate immune changes in depression, and likewise, immune processes can mediate chronobiological disruption. This may suggest a bi-directional relationship in immune-circadian crosstalk. Furthermore, given the immunomodulatory effects of antidepressants and chronotherapeutics, as well as their associated beneficial effects on circadian disturbance, we--and others--suggest that these therapeutic agents may exert their chronobiotic effects partially via the neuroimmune system. Further research is required to better elucidate the mechanisms of immune involvement in the chronobiology of depression.

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“…There is increasing evidence that T cells are actively involved in the modulation of neural and behavioral functions, with possible relevance to psychiatric conditions (Kipnis et al , 2004; Kipnis et al , 2008; Miller, 2010). In a model of in vivo activation of T cells with the superantigens staphylococcal enterotoxins A and B (SEA and SEB), it was shown that there is activation of selective areas of the brain involved in cognition and stress regulation (reviewed by Urbach-Ross & Kusnecov, 2009).…”

Section: Introductionmentioning

confidence: 99%

Effects of acute and repeated administration of Staphylococcal enterotoxin A on Morris water maze learning, corticosterone and hippocampal IL-1β and TNFα

Woodruff

Schorpp

Lawrenczyk

et al. 2011

Brain, Behavior, and Immunity

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Staphylococcal enterotoxin A (SEA) is a bacterial superantigen that induces pronounced T cell expansion and cytokine production. In addition, SEA activates the HPA axis and forebrain regions relevant to cognitive functions. Since learning-related cognitive changes have not been assessed in response to SEA, spatial learning in the morris water maze (MWM) was determined in male C57BL/6J mice subjected to acute or repeated injections of 5 μg SEA or Saline. Injections were given 2 hrs prior to 4–5 days of hidden platform sessions. Animals were then rested for 1 month and given retraining without further injections. In addition, splenic IL-1β, IL-2 and TNFα, plasma corticosterone, and hippocampal IL-1β and TNFα were measured after the regimen of treatment used in the behavioral experiments. The results showed no learning impairment following acute or repeated SEA challenge. Moreover, when retested one month later, and without further injections, the SEA group showed more rapid relearning of the MWM. This suggested that coincidental superantigenic T cell activation and training served to promote long-term improvement in recovery of learning. Furthermore, repeated SEA challenge continued to drive increases in plasma corticosterone, but with a compensatory reduction in hippocampal IL-1β. However, while hippocampal TNFα was reduced after acute and repeated SEA treatment, this was not statistically significant. In view of the importance of modest glucocorticoid elevations and hippocampal IL-1β in promoting contextual learning, the data point to the hypothesis that SEA promotes long-term plasticity by restraining disruptive increases in hippocampal IL-1β, and possibly TNFα, during learning.

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Immunity and cognition: what do age-related dementia, HIV-dementia and ‘chemo-brain’ have in common?

Cited by 76 publications

References 81 publications

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging

Reversal of Neuronal Atrophy: Role of Cellular Immunity in Neuroplasticity and Aging

Neuroimmunomodulation in unipolar depression: a focus on chronobiology and chronotherapeutics

Effects of acute and repeated administration of Staphylococcal enterotoxin A on Morris water maze learning, corticosterone and hippocampal IL-1β and TNFα

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