Dr. Hilbert Seeger

More evidence from scientists around the world:

Alzheimer's disease, Parkinson's disease, Motor Neurone disease, Diabetes Type II and some other common diseases are prion related.

Prion = Endobiont

Prof. Enderlein created remedies using endobionts of different fungal and bacterial species. These remedies carry therefore the risk of contributing to these diseases.

A modern scientific perspective on Enderlein's concept of microbial life cycles outlines an article by Ronald Ullman published in Townsend Letter for Doctors and Patients in May 2003. Read the article by clicking on the link below.  

http://findarticles.com/p/articles/mi_m0ISW/is_2003_May/ai_100767864

University of Melbourne, Bio21 Molecular Science and Biotechnical Institute

Excerpt from their recent paper: "Fighting Infections & Allergies" 

Transmissible Prion and Related Neurotoxic Diseases: The neurotoxicity and pathogenesis of ‘mad-cow’- causing prion, Alzheimer’s and Parkinson’s diseases are being investigated. For example, research on prion diseases, which are transmissible neurodegenerative disorders, aims to understand the processes by which the normal prion protein folds into the abnormal infectious form, giving rise to protein plaques characteristic of the neurodegenerative disorders. Related programs investigate Alzheimer’s-associated plaque-forming neurotoxic proteins and the role of metal ions in this process, as well as the design of inhibitors of plaque formation. From a public health perspective, a priority of these investigations is the development of rapid and sensitive diagnostic tests for prion infection and other plaque formation.

Read all at www.bio21.org

This article shows why Sanum remedies need to be tested for their safety:

Yeast prions [URE3] and [PSI⁺] are diseases

Toru Nakayashiki ^*, Cletus P. Kurtzman , Herman K. Edskes ^*, and Reed B. Wickner ^*, 

^*Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8, Room 225, Bethesda, MD 20892-0830; and Microbial Genomics and Bioprocessing Research Unit, National Center for Agricultural Utilization Research, Agricultural Research Service, United States Department of Agriculture, Peoria, IL 61604

Viruses, plasmids, and prions can spread in nature despite beinga burden to their hosts. Because a prion arises de novo in morethan one in 10⁶ yeast cells and spreads to all offspring inmeiosis, its absence in wild strains would imply that it hasa net deleterious effect on its host. Among 70 wild Saccharomycesstrains, we found the [PIN⁺] prion in 11 strains, but the [URE3]and [PSI⁺] prions were uniformly absent. In contrast, the "selfish"2µ DNA was in 38 wild strains and the selfish RNA repliconsL-BC, 20S, and 23S were found in 8, 14, and 1 strains, respectively.The absence of [URE3] and [PSI⁺] in wild strains indicates thateach prion has a net deleterious effect on its host.

Lethal viruses spread in wild host populations despite theirundesirable effects. The transmissible spongiform encephalopathyof sheep (scrapie) and the similar chronic wasting disease ofelk and deer are naturally infectious and spread despite oftendevastating effects on herds (1, 2). Chromosomal genes occasionallycheat on meiosis to promote their own spread despite unfavorableeffects on the host. The tail locus of mice, segregation distorterof Drosophila, and the spore killer of Neurospora, are welldocumented examples of alleles that prevent the inheritanceof the normal allele (3, 4). Retrotransposons litter mammaliangenomes although they rarely, if ever, pay their way by benefitingthe host (5, 6).

Laboratory strains of Sacharromyces cerevisiae harbor an arrayof nonchromosomal genetic elements, including mitochondrialDNA; the 2µ DNA plasmid; the L-A dsRNA virus and its toxin-encodingsatellite, M dsRNA; the single-stranded RNA replicons 20S RNAand 23S RNA (7, 8); and prions (infectious proteins) [URE3],[PSI⁺], [PIN⁺], and [ ] (9–11). [URE3], [PSI⁺], and [PIN⁺]are self-propagating amyloid forms of the Ure2, Sup35, and Rnq1proteins, respectively, whereas [] is the self-activating vacuolarprotease B. Mitochondrial DNA is an obvious benefit to its host,and the killer toxin production by the M dsRNA satellite ofthe L-A virus provides a rationale for the natural selectionof cells carrying L-A itself. However, the other nucleic acidelements all encode only viral coat proteins, RNA replicases,and other proteins promoting their own replication and segregation,and there is no known selective advantage of these replicons.

All of these elements are infectious in the sense that theyare transmitted horizontally from cell to cell by cytoplasmicmixing in mating. These elements generally segregate 4+:0 inmeiosis and are transmitted from donor to recipient in cytoduction(transient heterokaryon formation). Thus, like mammalian virusesor meiotic drive genes, the yeast prions, viruses, and plasmidsshould spread through wild populations unless (i) the wild populationhas never come in contact with the element or (ii) the elementis sufficiently disadvantageous that cells carrying it are selectedagainst.

Viruses or plasmids rarely arise de novo, so a geographicallyisolated Saccharomyces population may lack one of these onlybecause it has not encountered an infected, mating-compatiblehost. However there is no possibility that wild Saccharomycespopulations could be isolated from the yeast prions, becausethese elements arise de novo in one in 10⁶ cells. Thus the absenceof a prion in wild strains would be a strong indication thatit is a net disadvantage to its host.

Although most [URE3] strains show noticeably slowed growth andincreased sensitivity to Cd²⁺ and Ni²⁺ (12), it was reportedthat ure2 cells reached a slightly higher cell density undersome conditions (13) and allow better tolerance of Na⁺, Li⁺,and Mn²⁺ (14), and it was suggested that [URE3] may thus beadvantageous to yeast cells (15).

It has been proposed that the [PSI⁺] prion is advantageous tothe host, either to resist stress from heat or high ethanolconcentration (16) or to adapt to various environments (17).A range of conditions comparing pairs of [PSI⁺] and [psi^-] strainswas studied. Most conditions favored the [psi^-] strains, butthere were some conditions under which the [PSI⁺] member ofa pair was favored. Whether [PSI⁺] is an advantage or a disadvantagedepends on whether the conditions under which [PSI⁺] is favoredrepresent a significant part of the yeast ecological niche (18).Similar considerations apply to [URE3]. Thus, the range of theseprions in nature is a critical measure of their net benefitor detriment to their host. Nine clinical isolates of S. cereivisiaehave been previously examined and found to lack [PSI⁺], andtwo carried [PIN⁺] (19). However, Saccharomyces is only occasionallypathogenic for humans, so this niche is rather specialized forthis species. Chernoff et al. (20) examined two industrial strainsof S. cerevisiae and one each of eight other Saccharomyces speciesand found that none carried [PSI⁺]. We have examined 70 wildstrains and found neither [URE3] nor [PSI⁺]; however, 11 carriedthe [PIN⁺] prion. A comparison with "selfish" yeast virusesand plasmids provides standards for what should be expectedfor parasitic replicons (diseases of yeast).

Read it all at http://www.pnas.org/cgi/content/full/102/30/10575