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efta-efta00965007DOJ Data Set 9Other

From: Jeffrey Epstein <jeevacation®gmail.com>

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DOJ Data Set 9
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From: Jeffrey Epstein <jeevacation®gmail.com> To: ' Subject: Fwd: amyloid increases homocysteic acid toxicity Date: Wed, 17 Jul 2013 09:20:13 +0000 Forwarded message From: Date: Tuesday, July 16, 2013 Subject: Fwd: amyloid increases homocysteic acid toxicity To: Jeffrey Epstein <[email protected]> Forwarded message From: Tohru Date: Tue, Jul 16, 2013 at 7:00 PM Suliect: amyloid increases homocysteic acid toxicity To: Dear Christina; I am afraid Jeffrey has a question about the relationship between amyloid beta and homocysteic acid in blood for Alzheimer's disease process. Amyloid hypothesis is still valid for preventing AD. We already observed that homocysteic acid toxicity, especially, neurodegenerative toxicity, will increase in the presence of amyloid. However it has been observed that amyloid protein is present in normal brain, which shows that amyloid itself has no toxicity for brain work. Homocysteic acid has the original pathogen for AD process. Early onset of AD, familial AD, has higher production of amyloid, which increases the homocysteic acid toxicity, then very lower level of homocysteic acid can start the disease process. Recent reports indicate that ApoE4 increases the permeability of blood brain barrier, which allows the invasion of lower level of homocysteic acid in blood into brain. This my hypothesis is strongly supported by my TSH1 recovery, because TSH1 decreased homocysteic acid level in blood and blocked homocysteic acid toxicity in brain. EFTA00965007 Now I am sincerely request your support. Sincerely yours Tohru The information contained in this communication is confidential, may be attorney-client privileged, may constitute inside information, and is intended only for the use of the addressee. It is the property of Jeffrey Epstein Unauthorized use, disclosure or copying of this communication or any part thereof is strictly prohibited and may be unlawful. If you have received this communication in error, please notify us immediately by return e-mail or by e-mail to [email protected], and destroy this communication and all copies thereof, including all attachments. copyright -all rights reserved EFTA00965008

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