Advances in Brain Research

Brain research has had a long and productive history. The first efforts were to understand the normal human brain. Much of this was done by Wundt, Cajal, Rolando, Golgi, and others.

Scioli (1909)

Scioli studied the brains of patients with "dementia praecox" posthumously. Positive findings were reported including an increase in fat in brain cells, glial proliferation, and ameboid cells. Alzheimer of Germany reported similar dfindings in "dementia praecox", but reported different findings including plaques and tangles in the disease that now bears his name.

Jakob & Pedace (1938)

In 1938 an Argentinian group reported lysis of the cytoplasm with vacuolization in schizophrenia. They called it "plasmocytolysis".

the cytoplasm was blowing up like a balloon and bursting (lysis). Vacuoles are used by animal cells to store food or fat. In plant cells they can store water.

Swelling of the Oligodendroglia

This finding has been reported by a number of researchers including Cardona (1947), Elvidge & Reed (1938), Kirschbaum & Heilbrunn (1944), and Uranova (2001). Elvidge & Reed Kirschbaum & Heilbrunn used biopsies.

Alzheimer (1897, 1900, 1913)

Alzheimer published a series of reports on "dementia praecox". He found ameboid glia, fat deposits, pigment deposits, and cell loss.

Papez & Papez (1956)

Unfortunately James Papez died not long after this report. This group reported "drops of protein" in "clouded & catatonic states". In 1959 one of James Papez' reports was published posthumously. He found amyloid (starch) bodies in the brain in schizophrenia. This neuroanatomist became famous for his theory of emotion in relation to brain anatomy. He felt that subcortical parts of the brain were involved in emotions. This makes sense if one considers that animal have fear and rage like we do.

Averback (1981a, 1981b)

In two brilliant 1981 papers Averback reported studies of schizophrenia, Alzheimer's disease, and Huntington's chorea. He found subcortical pathology in all three diseases. Alzheimer's disease and Huntington's chorea are known to be neurodegenerative diseases. He found massive bloating & death of neurons with fat & pigment deposits, confirming Alzheimer. This strongly suggests that schizophrenia is also a neurodegenerative disease.

Averback also reported destruction of the Nissl bodies, which were "barely recognizable".

Drugs

Unfortunately many psychiatric drugs have had disastrous, including fatal, side effects. See references 3, 4, and 5.

Conclusions

The fat deposits reported by Alzheimer, Averback, and others suggest that the brain cells may be overeating. The destruction of the Nissl bodies suggests that the culprits are amino acids, which are housed in the Nissl bodies. All of this suggests that a diet very low in amino acids should be considered as a therapy.

More research needs to be done. The drugs that are in current use are not good enough. They are very expensive and too problematic.

References

1.

Lesions of the nucleus ansae peduncularis in neuropsychiatric disease.

Averback P.

Arch Neurol. 1981 Apr;38(4):230-5.

2.

Structural lesions of the brain in young schizophrenics.

Averback P.

Can J Neurol Sci. 1981 Feb;8(1):73-6.

3.

Extrapyramidal side-effects of antipsychotics in a randomised trial.

Miller del D, Caroff SN, Davis SM, Rosenheck RA, McEvoy JP, Saltz BL, Riggio S, Chakos MH, Swartz MS, Keefe RS, Stroup TS, Lieberman JA; Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators.

Br J Psychiatry. 2008 Oct;193(4):279-88.

4.

Fatal toxic epidermal necrolysis induced by carbamazepine treatment in a patient who previously had carbamazepine-induced Stevens-Johnson syndrome.

Huang LY, Liao WC, Chiou CC, Lou JP, Hu P, Ko FC.

J Formos Med Assoc. 2007 Dec;106(12):1032-7.

5.

Clozapine-induced angioneurotic edema.

Mishra B, Sahoo S, Sarkar S, Akhtar S.

Gen Hosp Psychiatry. 2007 Jan-Feb;29(1):78-80.