Research Findings

RESEARCH FINDINGS

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We employ a patented, non-surgical intranasal process to administer Transforming Growth Factor-alpha (TGFα) an endogenous, 50 amino acid protein.

Animal studies have demonstrated that TGFα causes the proliferation of massive numbers of adult neural stem cells in the brain. These new cells migrate to the locus of damage, differentiate into the kinds of cells that were lost, and re-establish lost connections, thereby repairing the damaged brain.

TGFα may be an important endogenous trophic factor in both central and peripheral tissues throughout development, adulthood, and in response to injury and degeneration of tissue.

In vivo induction of massive proliferation, directed migration, and differentiation of neural cells in the adult mammalian brain James Fallon, et al., 2000

Studies show that the transplanted proprietary cells, as other companies had thought, do not replace the original, lost cells; instead, the transplanted cells almost invariably die. Cell death is known to trigger the brain to express growth factors. It is these growth factors that cause the recovery sometimes seen in clinical trials of transplanted cells.

Proliferation and migration of neural stem cells induced
by intranasal administration of PEG-TGFα

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Immunofluorescent double-label images of coronal brain sections,
two months post-MCAO in adult rats. (A, D, and G)

A control animal that received only PBS after the MCAO. The
hemisphere ipsilateral to the MCAO infarct is depicted and stained
for both BrdU incorporation and nestin. (B, E, and H)

The ipsilateral hemisphere of an animal that received one weekly
intranasal treatment of 20 mg of PEG-TGFα for
4 weeks, stained for both BrdU and nestin. (C, F, and I)

The same hemisphere in an animal that received direct intracranial
infusion of 20 mg of TGFα over a 4-week period. In (I), the lesion site
lies outside the frame of the image.

(Scale bar: 500 mm.) LV, lateral ventricle; C-P, caudate putamen; CC,
corpus callosum; S, septum; SVZ, subventricular zone.