Re: Are you suffering from brain mold?

August 30, 2007

Hopefully, many of us can write about our problems with mold on this blog.

It is an opportunity for us to be heard!!

August 30, 2007

yes it is and dont forget to put your city and state down so that they know we

are from all across the states, and first name if you dont want to put your full

name

When I posted, I didnt realize it wouldnt put ask for my name and location until

after I posted, but I will be writing an email to him Darlene

ssr3351@... wrote:

Hopefully, many of us can write about our problems with mold on this blog.

It is an opportunity for us to be heard!!

---------------------------------

Moody friends. Drama queens. Your life? Nope! - their life, your story.

Play Sims Stories at Games.

August 30, 2007

I think that there is a strong possibility that the link between mold

exposure and depression is caused by the mechanism described by

There is an excellent free article in the Mt. Sinai Journal of Medicine on

" Neurogenesis in Adult Brain and Neuropsychiatric Disorders " at

Full text is at http://www.mssm.edu/msjournal/73/73_7_pages_931_940.pdf ,

I've pasted just the abstract below. And then I've pasted several abstracts

that I think show the connection between mold, hippocampal neurogenesis, and

depression...

Mt Sinai J Med. <javascript:AL_get(this, 'jour', 'Mt Sinai J Med.');> 2006

Nov;73(7):931-40.Links <javascript:PopUpMenu2_Set(Menu17195878);>

Research update: neurogenesis in adult brain and neuropsychiatric disorders.

*Elder

GA*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22Elder%\

20GA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstractPlus>,

*De Gasperi

R*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22De%20Ga\

speri%20R%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.\

Pubmed_RVAbstractPlus>,

*Gama Sosa

MA*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22Gama%2\

0Sosa%20MA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel\

..Pubmed_RVAbstractPlus>

..

Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA.

gregory.elder@...

Until recently neurogenesis in mammals was considered to occur only during

the embryonic and early post-natal periods and to have no significant role

in the adult nervous system. However, it is now accepted that neurogenesis

occurs in two brain regions in adult mammals, namely, the hippocampus and

olfactory bulb. In both regions new neurons arise from a resident population

of neural progenitor cells that are maintained throughout adult life.

Hippocampal neurogenesis is required for some types of hippocampal-dependent

learning. Many factors enhance hippocampal neurogenesis including hormones,

growth factors, drugs, neurotransmitters, and physical exercise as well as

learning a hippocampal-dependent task. Other factors suppress hippocampal

neurogenesis; these include aging, stress, glucocorticoids and stimuli that

activate the pituitary/adrenal axis. Recently much attention has become

focused on the relevance of hippocampal neurogenesis to the pathophysiology

and treatment of mood disorders. Indeed all major pharmacological and

non-pharmacological treatments for depression enhance hippocampal

neurogenesis and suppressing hippocampal neurogenesis in mice blocks

behavioral responses in some antidepressant-sensitive tests. Altered

hippocampal neurogenesis may also play a pathophysiological role in

neurodegenerative disorders such as Alzheimer's disease. How much

neurogenesis occurs normally in other brain regions is unclear. Neural

progenitors are found throughout the neuraxis including both neurogenic and

non-neurogenic regions. When cultured in vitro or isolated and transplanted

back into neurogenic brain regions, these cells can differentiate into

neurons although in their in situ location they seem to behave as

lineage-restricted glial progenitors. The environmental cues that limit the

potential of progenitor cells in non-neurogenic brain regions are unknown.

However, an emerging view is that astrocytes, a subset of which also

functions as neural progenitor cells, are critical in regulating the local

environment. After transplantation into adult brain, neural stem cells are

capable of surviving and differentiating into both neurons and glial cells,

offering hope that stem cell therapy may be utilized to treat a variety of

neurological and perhaps psychiatric disorders. The widespread existence of

endogenous neural progenitors even in non-neurogenic brain regions also

offers hope that the potential of these cells may be harnessed to repair

cellular injuries caused by injuries such as stroke, trauma or

neurodegenerative diseases. While obstacles remain to both approaches,

stem-cell-based therapies remain an area of intense research interest.

PMID: 17195878 [PubMed - indexed for MEDLINE]

Toxicol Sci. <javascript:AL_get(this, 'jour', 'Toxicol Sci.');> 2007

Jul;98(1):187-97. Epub 2007 Apr 21.

Links<javascript:PopUpMenu2_Set(Menu17449898);>

Adult hippocampal neural stem/progenitor cells in vitro are vulnerable to

the mycotoxin ochratoxin-A.*Sava

V*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22Sava%20\

V%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstractPlus>,

*Velasquez

A*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22Velasqu\

ez%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pub\

med_RVAbstractPlus>,

*Song

S*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22Song%20\

S%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstractPlus>,

*-Ramos

J*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed & Cmd=Search & Term=%22\

-Ramos%20J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel\

..Pubmed_RVAbstractPlus>

..

Department of Neurology, University of South Florida, Haley VA

Hospital, Tampa, Florida 33612, USA.

The common mycotoxin ochratoxin-A (OTA) accumulates in brain, causes

oxidative stress, and elicits a DNA repair response that varies across brain

regions and neuronal populations. Neural stem/progenitor cells (NSCs)

prepared from hippocampus of adult mouse brain were tested for their

vulnerability to the toxin in vitro. The following measurements were made in

NSC cell cultures in both proliferation and differentiation media: (1)

viability (trypan blue exclusion), (2) proliferative activity

([(3)H]-thymidine uptake), (3) the DNA repair response (oxyguanosine

glycosylase activity), and (4) antioxidative response (superoxide

dismutase). Cells that had proliferated to 90-100% confluency in the

presence of epidermal growth factor and basic fibroblast growth factor were

induced to differentiate by removal of the growth factors. OTA, added to the

cultures in concentrations of 0.01-100 microg/ml, caused a dose- and

time-dependent (6-72 h) decrease in viability of both proliferating and

differentiating NSC. Proliferating NSC exhibited a greater vulnerability to

the toxin than differentiated neurons despite robust DNA repair and

antioxidative responses. Preconditioning of NSC with a 12-h incubation with

the pro-oxidant diethyl maleate increased DNA repair activity and,

subsequently, provided a moderate degree of neuroprotection. Overall, these

results lead to speculation that OTA exposure may contribute to impaired

hippocampal neurogenesis in vivo, resulting in depression and memory

deficits, conditions reported to be linked to mycotoxin exposure in humans.

PMID: 17449898 [PubMed - in process]

..........

Neurotoxicology. <javascript:AL_get(this, 'jour', 'Neurotoxicology.');> 2006

Jan;27(1):82-92. Epub 2005 Sep 2.

Links<javascript:PopUpMenu2_Set(Menu16140385);>

Acute neurotoxic effects of the fungal metabolite ochratoxin-A.*Sava

V*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Sava%20\

V%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_R\

VAbstractPlus>,

*Reunova

O*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Reunova\

%20O%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubme\

d_RVAbstractPlus>,

*Velasquez

A*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Velasqu\

ez%20A%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pub\

med_RVAbstractPlus>,

*Harbison

R*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Harbiso\

n%20R%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubm\

ed_RVAbstractPlus>,

*Sánchez-Ramos

J*<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22S%C3%A1\

nchez-Ramos%20J%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_Results\

Panel.Pubmed_RVAbstractPlus>

..

University of South Florida, Department of Neurology (MDC 55), 12901 Bruce

B. Downs Blvd., Tampa, FL 33612, USA.

Ochratoxin-A (OTA) is a fungal metabolite with potential toxic effects on

the central nervous system that have not yet been fully characterized. OTA

has complex mechanisms of action that include evocation of oxidative stress,

bioenergetic compromise, inhibition of protein synthesis, production of DNA

single-strand breaks and formation of OTA-DNA adducts. The time course of

acute effects of OTA were investigated in the context of DNA damage, DNA

repair and global oxidative stress across six brain regions. Oxidative DNA

damage, as measured with the " comet assay " , was significantly increased in

the six brain regions at all time points up to 72 h, with peak effects noted

at 24 h in midbrain (MB), CP (caudate/putamen) and HP (hippocampus).

Oxidative DNA repair activity (oxyguanosine glycosylase or OGG1) was

inhibited in all regions at 6 h, but recovered to control levels in

cerebellum (CB) by 72 h, and showed a trend to recovery in other regions of

brain. Other indices of oxidative stress were also elevated. Lipid

peroxidation and superoxide dismutase (SOD) increased over time throughout

the brain. In light of the known vulnerability of the nigro-striatal

dopaminergic neurons to oxidative stress, levels of striatal dopamine (DA)

and its metabolites were also measured. Administration of OTA (0-6 mg/kg i.p.)

to mice resulted in a dose-dependent decrease in striatal DA content and

turnover with an ED50 of 3.2 mg/kg. A single dose of 3.5 mg/kg decreased the

intensity of tyrosine hydroxylase immunoreactivity (TH(+)) in fibers of

striatum, TH(+) cells in substantia nigra (SN) and TH(+) cells of the locus

ceruleus. TUNEL staining did not reveal apoptotic profiles in MB, CP or in

other brain regions and did not alter DARPP32 immunoreactivity in striatum.

In conclusion, OTA caused acute depletion of striatal DA on a background of

globally increased oxidative stress and transient inhibition of oxidative

DNA repair.

PMID: 16140385 [PubMed - indexed for MEDLINE]

There has been other research done on this too.. these were just the easiest

to find...

August 31, 2007

Hummmmm,

This was in the news this morning saying all you say below and showed very bad

mold in Florida Media.

You all are Great keep up the good work.

Peace

Elvira

LiveSimply <quackadillian@...> wrote: