Posted by stjames on August 27, 2000, at 22:18:39
Take heart Cam, thanks to you I found this great study !
http://www.elsevier.nl/gej-ng/10/33/33/32/33/26/article.html
"The neurodegeneration hypothesis proposes that schizophrenia is the result of degeneration or loss of neurons, similar to Alzheimer's disease. This hypothesis dates
to 1919, when schizophrenia was referred to as "dementia praecox" (Kraepelin 1919). However, post-mortem studies have not consistently identified evidence of
abnormal neurodegeneration in schizophrenic brains (Arnold et al. 1991).An alternative hypothesis states that the pathology of schizophrenia arises during embryonic and fetal developmental (Bloom 1993; Saugstad 1989). In this
hypothesis, Weinberger (Weinberger 1987) proposes that a static brain lesion is established early in development and that neurodegeneration is not a major factor in
the adult pathology. As the brain matures, it compensates for the lesion until the adaptations are overwhelmed. When the brain adaptions are insufficient to
compensate, the final groups of behavioral symptoms are collectively described as schizophrenia. As in the neurodegenerative hypothesis, supporting data are
circumstantial (Raedler et al. 1998).In bipolar illness, less is known about brain pathology than with schizophrenia. Consistent findings include mood state-dependent changes in erythrocyte
Na-K-ATPase activity (Looney and el-Mallakh 1997) and an increased risk for structural brain abnormalities (Altshuler et al. 1995). Both types of studies may
indicate subtle neuronal damage. A question raised by both schizophrenia and bipolar studies is whether there is ongoing neuronal damage or degeneration.The direct approach to test the hypothesis that schizophrenia and bipolar illness are not associated with ongoing neurodegeneration is to study neuronal tissue from
living patients. However, moral and ethical restrictions eliminate this type of study. One way to bypass this limitation is to study a protein that has been demonstrated
to be involved with the adult post-mortem pathology and can be measured in living subjects. Synaptosomal-associated protein 25kDa (SNAP-25) is a candidate
protein for this type of study. We recently reported identifying this protein in human cerebral spinal fluid (CSF)(Thompson et al. 1998a), and SNAP-25 belongs to
an important class of proteins involved with regulated neurotransmitter vesicle trafficking (Scheller 1995; Sollner et al. 1993). SNAP-25 is found primarily in the
central nervous system and is a T-SNARE (Jacobsson et al. 1996; Roth and Burgoune 1997; Oyler et al. 1989). In human post-mortem schizophrenic cortex
(Thompson et al. 1998b) the SNAP-25 levels are altered, and in an animal model of neuronal damage (Jorgensen et al. 1997), the level of SNAP-25 is decreased
initially after a trauma."james
poster:stjames
thread:43873
URL: http://www.dr-bob.org/babble/20000822/msgs/43873.html