[Neuroscience] The Neuroimmunology of Psychiatric Disorders

John H. via neur-sci%40net.bio.net (by j_hasenkam At yahoo.com.au)
Wed Nov 22 06:41:31 EST 2006

Hey Troops,

This is fast and messy extract from an email I've forwarded to a friend
attending a conference on neuroimmunology. I'll throw it up for those
interested in this fascinating area of research that is receiving
increasing attention. For those familiar with the subject the below
notes will provide some useful references. For those interested, the
work of Susan Swedo on PANDAS is very interesting.

22/11/2006 9:10PM

Frank, The Horrobin paper I have is extremely relevant to this. For
example, he cites one study where iv administration of pge1 can have a
remarkably quick effect on treating depression. He also states that
DRD2 occupation is the primary driver PLA2 synthesis, which is a
primary driver of Arachidonic acid production. Hmmm ... I wonder if ECT
has any impact on neuroimmune dynamics .... .9(see below, some promise
there)  Actually just today I read that the first antipsychotic, chlora
... is an antihistamine. The antidepressant I was taking,
mirtazapine(spelling), is a strong antihistamine. Also, I have a review
paper, very interesting, title is from memory: Cytokines and
Depression, the Need for a new paradigm, Can dig up if you wish.
Eyesight still steady, some fluctuations but improving. John.
22/11/2006 8:37PM
Some interesting stuff below, my guess, as usual, was sort of getting
there but not good enough. In notes below I refer to stuff in my
personal archives, can provide refs if you wish. Can also provide
Horrobin paper, I think this is very relevant. Might also be worth
looking any papers from Andrew Stoll guy, who did the omega 3 research
at Harvard.
EntrezECT and immunology, 56 hits - mostly because ECT also refers to
something else dammit.
J ECT 2005, mar, 21, (1): 52
j ect 2004 SEP;20(3): 197-8
Inflammation and depression: further studies are needed.
PMID: 15791184 [PubMed - indexed for MEDLINE]
Tumor necrosis factor-alpha, depression, and ECT: toward a better
understanding of the relationships.
PMID: 15343006 [PubMed - indexed for MEDLINE]
Raised plasma levels of tumor necrosis factor alpha in patients with
depression: normalization during electroconvulsive therapy.
PMID: 14657769
In the below lithium solved the problem, note that lithium helps in
both mania and depression, and robustly increases bcl 2! antiapoptotic.
Significant given recent research indicating that in bipolar there is
tissue destruction occurring.
A neuroimmune hypothesis for the aetiopathology of viral illness and
manic depression: a case report of an adolescent
PMID: 8835648
In this one, high interferon response from immune cells(in vitro).
Confounder, interferon for MS, though the benefit is typically small.
Need to look at IFNs in relation to how these can induce shift to Th 1
type, non-inflammatory response. Note that MS is typically perceived as
a Th 1 mediated autoimmune response, though I have read a microarray
study indicating Th 2 activity. I think, vaguely from memory, that in
MS you will see a reduction in HMG CoA, rate limiter for COQ10, the
important in preserving electron transport chain function.

Interferon responses in schizophrenia and major depressive disorders.
PMID: 7517191

This may relate to the hypothesis that some lymphocytes are regulatory:
suppressing inflammation, possibly via il4 and 10.

Immune changes induced by electroconvulsive therapy (ECT).
There is a significant increase in the percentage and absolute number
of activated lymphocytes (OKT10+, IL2R1+) after ECT treatment of major
depressive disorder. There is an acute decrease in the absolute number
of total lymphocytes, T8+ and Leu11+ cells one hour after a single ECT.
PMID: 1605490 [PubMed -
Fascinating, have one abstract in archives demonstrating high titer of
autoantibodies to hsp60 in schizophrenia. This reminds of research
demonstrating high titer of IGG (found in this study also) in relation
to alz. Also, Pollmacher finding that in a subset of schizophrenics
neocortical inflammation prior to psychosis onset. also from
Pollmacher, even very low levels of LPS, insufficient to create
sickness behavior, can induce subtle cognitive deficits.

Abnormal cerebrospinal fluid protein indices in schizophrenia.
PMID: 4041510
Cannot make any sense of this below caffeine, a non-selective
antagonist of adenosine receptors, is neuroprotective. Also recent
research indicates coffee good for inhibiting onset of Diabetes 11,
though this may relate to potent antioxidant content (carotenes and
polyphenols) in coffee. There is emerging evidence to suggest that
diabetes has a significant inflammatory component, entirely concordant
with the pathologies that can occur with sustained diabetes 11.

ECT AND microglia, one hit
The role of glial adenosine receptors in neural resilience and the
neurobiology of mood disorders.
Adenosine receptors were classified into A1- and A2-receptors in the
laboratory of Bernd Hamprecht more than 25 years ago. Adenosine
receptors are instrumental to the neurotrophic effects of glia cells.
Both microglia and astrocytes release after stimulation via adenosine
receptors factors that are important for neuronal survival and growth.
Neuronal resilience is now considered as of pivotal importance in the
neurobiology of mood disorders and their treatment. Both sleep
deprivation and electroconvulsive therapy, two effective therapeutic
measures in mood disorders, are associated with an increase of
adenosine and upregulation of adenosine A1-receptors in the brain.
Parameters closely related to adenosine receptor activation such as
cerebral metabolic rate and delta power in the sleep EEG provide
indirect evidence that adenosinergic signaling may be associated with
the therapeutic response to these measures. Thus, neurotrophic effects
evoked by adenosine receptors might be important in the mechanism of
action of ECT and perhaps also sleep deprivation.
PMID: 16341582 [PubMed - indexed for MEDLINE]

Subject: Neuroimmune stuff at Academy, Dec. 13


Immune-Mediated Neuropsychiatric Disorders
Speakers: Susan Swedo, National Institutes of Mental
Health, NIH; Andy Miller, Emory University; Betty Diamond,
Columbia University
Sponsored by: Neuroimmunology Discussion Group
Organizers: Mady Hornig, Columbia University; Betty
Diamond, Columbia University

The Neuroimmunology Discussion Group focuses on the
interface between the immune system and the nervous system
both in the brain and in the periphery, in normal and
pathological conditions. This highly interdisciplinary
group seeks to bring together immunologists and
neuroscientists interested in exploring the intersection of
these two fields in periodic meetings that will include
discussions of basic, clinical, and translational aspects
of this emerging field.

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