Schizophrenia as Neuronal Disease

Introduction

  Schizophrenia is a disease of both the neurons & glia. Other forms of mental illness are similar. "Dementia praecox" is simply an old name for what is now called "schizophrenia".

Gliosis

"Stevens (1982), in keeping with observations going back as far as Alzheimer (Nieto and Escobar, 1972; Fisman, 1975), found fibrillary gliosis (reactive astrocytosis) in ~70% of her cases of schizophrenia. The gliosis was usually located in periventricular and subependymal regions of the diencephalon or in adjacent basal forebrain structures. As gliosis is a sign of past inflammation (Kreutzberg et al., 1997), this finding supported a number of aetiopathogenic scenarios for schizophrenia involving infective, ischaemic, autoimmune or neurodegenerative processes."

Harrison (1999)

  My own interpretation is that schizophrenia is a neurodegenerative disease. Gliosis proves that the popular, but false, neurodegenerative theory is wrong. Toxic diseases show gliosis. It signifies that schizophrenia is caused by an unknown toxic factor or factors.

Stevens (1982)

  This otherwise brilliant report did not mention two 1981 papers by Averback showing positive findings in schizophrenia, Alzheimer's disease, and Huntington's chorea. The findings were similar in all three diseases.

  Stevens reported a number of positive findings including corpora amylacea, gliosis (subcortical), mineralization, etc. Corpora amylacea are starch bodies indicating a slowing of glucose metabolism, which is vital to the brain. I find this to be an important clue which has been ignored by other reviewers such as Harrison (1999). But what causes the slowing of glucose metabolism, which is vital to the brain?

Averback (1981a, 1981b)

  Averback consistently found pathology in "young" schizophrenics in these postmortem studies. Pathology was found in the septal area and in the nucleus ansae peduncularis (part of the substantia innominata). Both areas are subcortical, which is consistent with subcortical pathology reported by Stevens (1982) and earlier by Nieto & Escobar.

  Averback found massive bloating & death of neurons with large fat vacuoles and pigment deposits. He thought that the pigment was lipofuscin. He found that the Nissl bodies were "barely recognizable", indicating destruction of the Nissl substance. The Nissl substance contains amino acids. If amino acids flooded the cells, these findings would be explained. Some of the excess amino acids would be converted to fat, explaining the fat vacuoles and the bloating & death of the neurons. The Nissl substance probably could not handle the excess amino acids.

Conclusions

  My amino acid theory also explains the findings of Stevens. If excessive amino acids are flooding the cells, the cells are likely to burn them instead of glucose just to get rid of them. The brain can't burn fat. With the brain burning amino acids for fuel, the starch deposits (corpora amylacea) would be explained. Similar deposits were previously reported by Dr. James Papez.

  But what is to be done about it? My recommendation is a diet very low in amino acids and possibly also low in fat. The neurons are blowing up like ballooons and bursting. Some unknown toxin is causing these things to happen. The toxin needs to be identified and destroyed, if possible. It could be a stress chemical since stress is known to make schizophrenia worse. For more information, consult the bibliography as well as my other articles. 

Bibliography

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