Glial Cell Loss in the Anterior Cingulate Cortex, a Subregion of the Prefrontal Cortex, in Subjects With Schizophrenia

Anette K. Stark, Harry B.M. Uylings, Ernesto Sanz-Arigita, Bente Pakkenberg
AJP. 2004-05-01; 161(5): 882-888
DOI: 10.1176/appi.ajp.161.5.882

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1. Am J Psychiatry. 2004 May;161(5):882-8.

Glial cell loss in the anterior cingulate cortex, a subregion of the prefrontal
cortex, in subjects with schizophrenia.

Stark AK(1), Uylings HB, Sanz-Arigita E, Pakkenberg B.

Author information:
(1)Research Laboratory for Stereology and Neuroscience, Bispebjerg Hospital,
Bispebjerg Bakke, 2400 Copenhagen NV, Denmark.

OBJECTIVE: Structural deficits in the anterior cingulate cortex such as changes
in glial cell and neuron numbers may be part of the anatomical substrate for
schizophrenia and need to be investigated. The total number of neurons and glial
cells in brains of 12 schizophrenia subjects and 14 comparison subjects were
determined in two subdivisions of the prefrontal cortex: Brodmann’s area 24, a
part of the anterior cingulate cortex, and Brodmann’s area 32 in the
paracingulate cortex.
METHOD: The estimate of the total cell number was obtained by multiplying the
volume of the region (estimated by using Cavalieri’s point counting method) by
the numerical density obtained from optical disectors in the
cytoarchitectonically defined areas from the prefrontal cortex.
RESULTS: The average total of bilateral glial cells in Brodmann’s area 24 was 201
x 10(6 )in subjects with schizophrenia and 302 x 10(6 )in comparison subjects, a
statistically significant difference of 33%, whereas there was a nonsignificant
difference between the schizophrenia subjects and the comparison subjects in
total number of glial cells in Brodmann’s area 32. The bilateral average total
number of neurons in areas 24 and 32 did not differ significantly between the
schizophrenia and comparison subjects.
CONCLUSIONS: A selective reduction in glial cells in Brodmann’s area 24 (but not
in area 32) is seen in brains of subjects with schizophrenia relative to those of
comparison subjects. Further investigations of the glial cells, their mutual
relationship, and their relationship with neurons are needed to understand the
role of specific glial components in this mental disorder.

DOI: 10.1176/appi.ajp.161.5.882
PMID: 15121654 [Indexed for MEDLINE]

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