I think the reason there is shrinkage in the Alzheimer's and Schizophrenic brain is due to the fact that this person's "cognitive model" is no longer effective, and as a result, they start losing connections in their brain...
Why I ask about neuron regeneration is, if an Alzheimer's patient or a Schizophrenic could develop a new cognitive (i.e. a new way to think about life) would new neuronal connections sprout as a result? Is this dependent on age? Could this be induced artificially? "naturally"?
I'm not even sure if I'm making sense...
BRB
Full Version: A theory about Alzheimer's and Schizophrenia...
I think this article is relevant to what you are asking about schizophrenia. I've pasted the summary from the end of the article.
http://www.acnp.org/g4/GN401000112/Default.htm
Neurodevelopmental Perspectives on Schizophrenia (2000)
Daniel R. Weinberger
http://www.acnp.org/g4/GN401000112/Default.htm
Neurodevelopmental Perspectives on Schizophrenia (2000)
Daniel R. Weinberger
QUOTE
OVERVIEW
The research summarized in this chapter tends, on the whole, toward the interpretation that individuals who manifest schizophrenia in early adult life have suffered some form of subtle cerebral maldevelopment in utero. This assumption is based on imperfect studies and inconclusive data. Nevertheless, there are a number of converging lines of evidence. The morphometric anatomical data from in vivo and postmortem investigations are difficult to attribute to a neuropathological process of adult life. The static nature of the structural findings, the correlations with early life adaptation, and the absence of gliosis are much more consistent with the possibility of a developmental anomaly. By far, the most important anatomical data concerns the evidence of cytoarchitectural disorganization of the cortex. These findings are virtually pathognomonic of a defect in cortical development occurring during the second trimester of gestation. If these data can be replicated in methodologically unimpeachable studies, a "smoking gun" will have been identified. Further efforts in this regard should be at the top of the list of priorities in schizophrenia research.
The other issues in thinking about schizophrenia as a neurodevelopmental disorder pivot on the validity of the cytoarchitectural findings. If these postmortem results are valid, then the etiology is one that affects brain development during this critical period. The etiology would clearly not be birth complications. Moreover, the question of why the clinical manifestations of such congenital damage are not present in recognizable form until early adulthood also becomes increasingly important, because answering this question may hold clues to the mechanisms of clinical compensation and decompensation. The scenario stressed in this chapter involves an interaction of cortical maldevelopment with normal programs of postnatal functional development of critical intracortical neural systems. The systems that appear to be especially relevant to the cortical functional impairments of schizophrenia involve prefrontal and limbic cortices and their connectivity. Such highly evolved, late maturing systems may be especially important in coping with the vicissitudes of independent psychosocial functioning and may be critical as well for the stress-related management of subcortical dopamine activity. As recently demonstrated in a new wave of heuristically meaningful animal models, it is conceivable that a congenital defect in such systems would remain submerged until early adult life and then fail to properly regulate critical secondary systems (e.g., subcortical dopamine activity) in the context of environmental stress. It is further conceivable that genetically determined variations in intracortical connectivity or in responsivity of the limbic dopamine system, which would not be clinically significant by themselves, could become clinically devastating when combined with the manner of cortical maldevelopment implicated above.
The research summarized in this chapter tends, on the whole, toward the interpretation that individuals who manifest schizophrenia in early adult life have suffered some form of subtle cerebral maldevelopment in utero. This assumption is based on imperfect studies and inconclusive data. Nevertheless, there are a number of converging lines of evidence. The morphometric anatomical data from in vivo and postmortem investigations are difficult to attribute to a neuropathological process of adult life. The static nature of the structural findings, the correlations with early life adaptation, and the absence of gliosis are much more consistent with the possibility of a developmental anomaly. By far, the most important anatomical data concerns the evidence of cytoarchitectural disorganization of the cortex. These findings are virtually pathognomonic of a defect in cortical development occurring during the second trimester of gestation. If these data can be replicated in methodologically unimpeachable studies, a "smoking gun" will have been identified. Further efforts in this regard should be at the top of the list of priorities in schizophrenia research.
The other issues in thinking about schizophrenia as a neurodevelopmental disorder pivot on the validity of the cytoarchitectural findings. If these postmortem results are valid, then the etiology is one that affects brain development during this critical period. The etiology would clearly not be birth complications. Moreover, the question of why the clinical manifestations of such congenital damage are not present in recognizable form until early adulthood also becomes increasingly important, because answering this question may hold clues to the mechanisms of clinical compensation and decompensation. The scenario stressed in this chapter involves an interaction of cortical maldevelopment with normal programs of postnatal functional development of critical intracortical neural systems. The systems that appear to be especially relevant to the cortical functional impairments of schizophrenia involve prefrontal and limbic cortices and their connectivity. Such highly evolved, late maturing systems may be especially important in coping with the vicissitudes of independent psychosocial functioning and may be critical as well for the stress-related management of subcortical dopamine activity. As recently demonstrated in a new wave of heuristically meaningful animal models, it is conceivable that a congenital defect in such systems would remain submerged until early adult life and then fail to properly regulate critical secondary systems (e.g., subcortical dopamine activity) in the context of environmental stress. It is further conceivable that genetically determined variations in intracortical connectivity or in responsivity of the limbic dopamine system, which would not be clinically significant by themselves, could become clinically devastating when combined with the manner of cortical maldevelopment implicated above.
From what I've experienced of Alzheimers the sufferer often seems to be living in different decades to the rest of us. They'll be with you one minute and the next they are asking when their dead spouse will be home, or they'll not understand that they don't live in the same house as they did 20 years ago.
It could be that memories are written in a linear and overlapping fashion. For instance, take cats for example. If you move house you have to keep the cat indoors or a very close watch for a few weeks maybe months before you begin to let it outside again. Otherwise the cat will go back to its old home.
I'm not sure if this conundrum has already been explained, but alzheimers seems to peel off layers of current memory and leave the sufferer with only 'current' memories of an earlier time. I've even heard of this going back as far as their teen years.
It could be that memories are written in a linear and overlapping fashion. For instance, take cats for example. If you move house you have to keep the cat indoors or a very close watch for a few weeks maybe months before you begin to let it outside again. Otherwise the cat will go back to its old home.
I'm not sure if this conundrum has already been explained, but alzheimers seems to peel off layers of current memory and leave the sufferer with only 'current' memories of an earlier time. I've even heard of this going back as far as their teen years.
Thanks Orbz...I'll get to reading it 1rst thing in the morning.
Although...what I have read from the Overview seems to indicate that the author thinks schizophrenia stems from a congenital defect in neural development.
My theory, however, is basically that schizophrenia as well as alzheimer's disease stem from some sort of disruption (or trauma) to "normal" neural development...Perhaps the schizophrenic's occurs earlier in life (not necessarily prenatally) than the alzhiemer's patient (and maybe this is the cause of the differing symptoms)...and my thought process stems from the observation that the two brains (schizophrenic and alzheimer's) appear similar comparatively (in my opinion) when displayed in post mortem exhibits by various researchers.
I don't know anything for certain...I don't even officially have my bachelor's degree yet, but these are the things I think about and I guess my ability to answer these questions conclusively or otherwise will determine my future in this field (or lack thereof...in reference to future).
I've gotta say, though, that I take exception to the author's use of the word "maldevelopment" with regards to the description of the early stages of the schizophrenic brain. Perhaps "atypical development" would be a better description (if my suggested description is even suitable for what the author observed...I guess I'll have to read the entire article myself to determine that)...anyway, by atypical, I mean "not consistent with that which is considered to be normal when taking the subject's developmental environment into consideration". So, what could be considered "normal" in Utah may not be considered "normal" in Washington, DC (for lack of a better analogy...haha)
OK, I'm going to officially "call it a night"...lol.
G'night, all. :-)
Although...what I have read from the Overview seems to indicate that the author thinks schizophrenia stems from a congenital defect in neural development.
My theory, however, is basically that schizophrenia as well as alzheimer's disease stem from some sort of disruption (or trauma) to "normal" neural development...Perhaps the schizophrenic's occurs earlier in life (not necessarily prenatally) than the alzhiemer's patient (and maybe this is the cause of the differing symptoms)...and my thought process stems from the observation that the two brains (schizophrenic and alzheimer's) appear similar comparatively (in my opinion) when displayed in post mortem exhibits by various researchers.
I don't know anything for certain...I don't even officially have my bachelor's degree yet, but these are the things I think about and I guess my ability to answer these questions conclusively or otherwise will determine my future in this field (or lack thereof...in reference to future).
I've gotta say, though, that I take exception to the author's use of the word "maldevelopment" with regards to the description of the early stages of the schizophrenic brain. Perhaps "atypical development" would be a better description (if my suggested description is even suitable for what the author observed...I guess I'll have to read the entire article myself to determine that)...anyway, by atypical, I mean "not consistent with that which is considered to be normal when taking the subject's developmental environment into consideration". So, what could be considered "normal" in Utah may not be considered "normal" in Washington, DC (for lack of a better analogy...haha)
OK, I'm going to officially "call it a night"...lol.
G'night, all. :-)
QUOTE(dutch84 @ Jan 23, 2008, 05:40 PM) 
Although...what I have read from the Overview seems to indicate that the author thinks schizophrenia stems from a congenital defect in neural development.
Certainly some kind of abnormality which possibly presents itself early behaviourally, but not as schizophrenia until late adolescence when the brain is undergoing a major pruning. If I remember correctly from the article, they suggest the brain wires itself abnormaly during development (for whatever reason; genetics, viral, stress, prenatal insult etc) which then manifests as schizophrenia later on when connections are pruned. These connections may have been responsible for keeping psychosis at bay (some kind of psychosis inhibitory system), until they're pruned (leaving no psychosis inhibitory system).
QUOTE
My theory, however, is basically that schizophrenia as well as alzheimer's disease stem from some sort of disruption (or trauma) to "normal" neural development...Perhaps the schizophrenic's occurs earlier in life (not necessarily prenatally) than the alzhiemer's patient (and maybe this is the cause of the differing symptoms)...and my thought process stems from the observation that the two brains (schizophrenic and alzheimer's) appear similar comparatively (in my opinion) when displayed in post mortem exhibits by various researchers.
Maybe. I don't know much about Alzheimer's, but its more about degradation of brain tissue (amyloid plaques and stuff) rather than faulty connections, which seems to be the case in Schizophrenia.
QUOTE(dutch84 @ Jan 20, 2008, 06:31 PM)
Why I ask about neuron regeneration is, if an Alzheimer's patient or a Schizophrenic could develop a new cognitive (i.e. a new way to think about life) would new neuronal connections sprout as a result? Is this dependent on age? Could this be induced artificially? "naturally"?
I think I remember from a seminar that more years of education reduces the risk of developing Alzheimer's. Use it or lose it.
September 07, 2004
Genetic Link between Schizophrenia and Alzheimers Found
Read more... Schizophrenia Biology
Gene found to be connected with Schizophrenia and to Alzheimer disease
This week Dr. D. Craig and colleagues, of Queens University Belfast, (Ireland) Department of Geriatric Medicine announced that they have found a link betweek the "Interleukin-1 beta" gene and Alzheimer disease.
However, the explanation for why some patients develop psychotic change in Alzheimer disease is still unclear.
"Psychosis-modifier genes" may act in the setting of neurodegeneration to
produce Alzheimer Disease plus psychosis in a similar way to how genetic modulation during neurodevelopment leads to schizophrenia," the scientists in North Ireland report.
"we tested the association between the functional interleukin-1beta -511 promoter polymorphism with delusions and hallucinations in Alzheimers" and found "Significant associations were found, thus confirming the previously noted increased risk in schizophrenia."
Source: Annals of Neurology (The interleukin 1 beta gene promoter polymorphism (-511) acts as a risk factor for psychosis in Alzheimer's dementia. Ann Neurol, 2004;56(1):121-124).
Genetic Link between Schizophrenia and Alzheimers Found
Read more... Schizophrenia Biology
Gene found to be connected with Schizophrenia and to Alzheimer disease
This week Dr. D. Craig and colleagues, of Queens University Belfast, (Ireland) Department of Geriatric Medicine announced that they have found a link betweek the "Interleukin-1 beta" gene and Alzheimer disease.
However, the explanation for why some patients develop psychotic change in Alzheimer disease is still unclear.
"Psychosis-modifier genes" may act in the setting of neurodegeneration to
produce Alzheimer Disease plus psychosis in a similar way to how genetic modulation during neurodevelopment leads to schizophrenia," the scientists in North Ireland report.
"we tested the association between the functional interleukin-1beta -511 promoter polymorphism with delusions and hallucinations in Alzheimers" and found "Significant associations were found, thus confirming the previously noted increased risk in schizophrenia."
Source: Annals of Neurology (The interleukin 1 beta gene promoter polymorphism (-511) acts as a risk factor for psychosis in Alzheimer's dementia. Ann Neurol, 2004;56(1):121-124).
Are there any Alzheimer's drugs that are also prescribed for schizophrenia?
QUOTE(dutch84 @ Jan 20, 2008, 01:31 PM)
Why I ask about neuron regeneration is, if an Alzheimer's patient or a Schizophrenic could develop a new cognitive (i.e. a new way to think about life) would new neuronal connections sprout as a result? Is this dependent on age? Could this be induced artificially? "naturally"?
Thank you for your post, but you're actually not right. The main cause of the Alzheimer's disease is not concerned with the uncertain death od neurons, but with the deposits of APP. Furthermore, there too many reasons to describe pathogenesis of schizophrenic syndromes, e.g. the hyperactivity of MAO or low levels of superoxyde dismutase, that will raise tardive dyskinesia symptoms.
I appreciate.
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