International Findings in Schizophrenia

Alzheimer (1897, 1913) reported positive findings in "dementia praecox". These findings were later confirmed by Southard (1914, 1915). He reported increased glial density. The report in 1913 was a study of 18 cases. There was neuronal loss primarily in layers 2 and 3 of the cortex. There was decreased neuropil. Southard found volume loss in the cortex. In 1910 he found internal hydrocephalus. There were temporal lesions. There was parietal atrophy and sclerosis in catatonia. Southard was from the United States. Alzheimer was from Germany.

Aganova & Uranova (1992)

This Russian group used the electron microscope to study schizophrenia. They reported swelling of synapses in layers 1 and 2 of area 24. This is a Brodmann area which is also called the anterior cingulate gyrus. Braitenberg (1952) found decreased staining of nerve cells with the Nissl stain. This was reported in layers 2 to 4 in schizophrenics.

Japanese Research

In 1993 Hirata Hibi & Hayashi reported the "P Lymphocyte", which they felt was "a stimulated atypical lymphocyte that is found in schizophrenics and some of their relatives". The cytoplasm contains vacuoles. The chromatin is abnormal. There are cytoplasmic granules.

German Research

Muller et al (1998) reported a case of "schizophrenia-like symptoms" in Wilson's disease. This disease has copper deposits in the liver and basal ganglia. There are also neurological symtoms. This suggests a possible link between schizophrenia and the basal ganglia, which are high in dopamine.

American Research

In 1952 Leon Roizin of New York reported a study on the histopathology of schizophrenia. He used biopsy material. Changes were seen in the Nissl bodies. "... the Nissl bodies were losing the clear-cut differentiation from the surrounding protoplasm as they were undergoing fragmentation, irregular pulverization, assuming finally an almost dust-like appearance." Some cells exhibited "marked central chromatolysis" and "ballooning of the cell body". "The highest degree of hypochromasy and staining pallor was observed in the most severe type of tigrolysis ..." Neurons were seen "undergoing degenerative changes". Neuronophagia was seen.

In 1998 in the American Journal of Psychiatry Keshavan et al reported decreased caudate volume in "neuroleptic naive psychotic patients".

More Russian Findings

Russian workers reported oligodendroglial cells demonstrated reactive and regressive changes, including swelling of cell cytoplasm and organelles, loss of mitochondria, vacuolization of the endoplasmic reticulum, etc. Oligodendroglial cell death was suggested.

Torrey et al (2000)

In 2000 Torrey et al reported ultrastructural alterations of the myelin sheath lamella in the frontal cortex of schizophrenic patients. Abnormalities included inclusions beween lamella of myelin sheaths, a loss of myelin sheath compactness, and the formation of concentric lamellar bodies. Similar findings were reported by Cotter et al in 2000. Orlovskaya et al (2000) reported abnormalities in both biopsy samples and autopsy samples. The 1972 work by Miyakawa et al was confirmed.

Averback

In 1981 P. Averback, who originated in Cambridge, England, published two brilliant reports. In a Canadian journal he reported "massive swollen neurons filled with lipid vacuolar and pigment material" in the nucleus ansae peduncularis and the septal nuclei in "young schizophrenics". Positive findings were reported in "13 of 13" from the schizophrenic group.

Averback reported "fragmentation of occasional cells", "abundant pigment in some cells", and various other findings. It would appear that the pigment might represent neuromelain or an abnormal variation of neuromelanin. The "masses of lipid droplets" in the "swollen neurons" appear to suggest that that the neurons are over-eating, so to speak. There may be some kind of transport error causing some macronutients (such as amino acids) to flood the cells. Since protein can be converted to fat, a flooding of the cells with amino acids would appear to explain some of the data. The "lipofuscin-like material" may be more difficult to explain. "Both septal and N. A. P. neurons were involved in all schizophrenic cases." Amazingly this brilliant work has been almost completely ignored because scientists did not understand it. Averback suggested that patients with "functional psychosis" in reality "have some form of organic brain disease". Since neuromelanin comes from dopamine metabolism, it is possible that an error in dopamine metabolism could cause both the transport error and the pigment accumulation.

Conclusions

Since the Nissl bodies house amino acids (for the purpose of synthesis of proteins), it would appear that an error in amino acid metabolism is taking place. A flooding of the cell with amino acids would explain the destruction of the Nissl bodies. If amino acids flood the cells, this could cause fat vacuoles. The cytoplasmic granules observed by the Japanese workers could be glycogen. Excess amino acids could be converted into fat. Excess amino acids could also be burned for fuel instead of glucose. This could cause an accumulation of glycogen. But what is to be done? More research is needed. Also it would seem that a diet very low in amino acids might help.

References

1. www.associatedcontent.com/article/602231/hoffers_laws_of_natural_nutrition_a.html .
2. www.associatedcontent.com/article/599867/linus_pauling_and_orthomolecular_medicine.html.

3. www.associatedcontent.com/article/597363/tryptophan_and_mental_illness.html.

4. www.associatedcontent.com/article/585783/the_human_brain_and_mental_illness.html.