Has anyone been able to get their sense of smell back?

[Guest guest]

I miss mine, and I think the lack of a sense of smell might be

effecting me in other ways too, so I am worried about that. Has anyone

ever really gotten theirs back after being in mold and losing theirs?

Also, I think this might apply to children as well as perhaps adults

living in moldy situations, at the very least NAC might at least

attenutate the injury caused by LPS's synergy with mycotoxins.

(oligodendrocyte progenitors also figure greatly in the 'chemo brain'

syndrome..and probably in post-mold brain fog)

(below)

J Neurosci Res. 2004 Nov 1;78(3):347-61.Click here to read Links

N-acetylcysteine prevents endotoxin-induced degeneration of

oligodendrocyte progenitors and hypomyelination in developing rat

brain.

Paintlia MK, Paintlia AS, Barbosa E, Singh I, Singh AK.

Department of Pediatrics, Medical University of South Carolina, 96

Lucas Street, ton, SC 29425, USA.

Periventricular leukomalacia (PVL), the dominant form of brain

injury in premature infants, is characterized by diffuse white matter

injury and is associated with cerebral palsy (CP). Maternal and

placental infections are major causes of prematurity and identifiable

etiology of PVL and CP. Here we have evaluated the therapeutic

efficacy of N-acetylcysteine (NAC), a potent antioxidant and precursor

of glutathione, to attenuate lipopolysaccharide (LPS)-induced white

matter injury and hypomyelination in the developing rat brain, an

animal model of PVL. Intraperitoneal pretreatment of pregnant female

rats with NAC (50 mg/kg), 2 hr prior to administration of LPS at

embryonic day 18 (E18), attenuated the LPS-induced expression of

inflammatory cytokines such as tumor necrosis factor-alpha,

interleukin-1beta, and inducible nitric oxide synthase in fetal rat

brains. There were significantly reduced numbers of TUNEL(+) nuclei

coimmunostained for platelet-derived growth factor-alphaR(+) [a

surface marker for oligodendrocyte progenitor cells (OPCs)] at E20 in

the subventricular zone of fetal rat brain in the NAC + LPS group

compared with the untreated LPS group. Interestingly, immunostaining

for O4 and O1 as markers for late OPCs and immature oligodendrocytes

demonstrated fewer O4(+) and O1(+) cells in the LPS group compared

with the NAC + LPS and control groups. Consistent with O4(+)/O1(+)

cell counts, the expression of myelin proteins such as myelin basic

protein, proteolipid protein, and 2'3'-cyclic nucleotide

phosphodiesterase, including transcription factors such as MyT1 and

Gtx, was less in the LPS group at late postnatal days, indicating

severe hypomyelination in the developing rat brain when compared with

NAC + LPS and control groups. Collectively, these data support the

hypothesis that NAC may provide neuroprotection and attenuate the

degeneration of OPCs against LPS evoked inflammatory response and

white matter injury in developing rat brain. Moreover, these data

suggest the possible use of NAC as a treatment for pregnant women with

maternal or placental infection as a means of minimizing the risk of

PVL and CP. Copyright 2004 Wiley-Liss, Inc.

PMID: 15389835 [PubMed - indexed for MEDLINE]