According to this paper, atypical antipsychotics can, if I understand it right, increase growth of brain cells which are lost due to psychosis and depression and SZ in general.
These things are so hard to get a grasp on. Seems like there are different studies with contradictory information constantly. Ap’s protect the brain, Ap’s cause brain shrinkage, Ap’s increase brain cell growth, Sz have increased brain age, Psychosis cause brain damage, Brain age is higher pre onset of sz symptoms does not increase later on with psychosis/length of disorder duration…etc etc…on and on it goes with contradictory information.
True, I did some more research and it seems like it is impossible to come up with a conclusion.
I guess the problem is, that SZ can cause deterioration of the brain and since people with SZ take AP’s it’s difficult to measure what causes the damage.
“As of January 2008, no studies have been published of neurogenesis with the SGAs aripiprazole and ziprasidone.”
Ooh, yeah. Uh. I started Geodon last November. I think after the first month, I experienced what could be described as hippocampal neurogenesis OR neurogenesis in the neurogenic regions, the olfactory epithelium and the subventricular zone, respectively. This euphoric neurotransmitter replenishment effect only lasted maybe 24 hours and hasn’t happened again, unfortunately. This regeneration of cortical gray matter felt incredible. My neuronal network increased in structure and function by possibly: generated dentate gyrus of the hippocampus, growth in neuropil surrounding the neurons, stimulated genesis of glial cells that pervades brain white matter, increases in nucleus accumbens, increases in superior and middle temporal gyri. This results in cortical or brain volume gains and brain tissue gains.
“SGAs may enhance synaptic connectivity, which could lead to repairing the diminished neuropil in the cortex of people with schizophrenia.”
I guess you are right @columbus . My pdoc keeps telling me that I should stay on the same kind of meds for a long period, but that’s difficult if you are noget having any effect of your meds
But now I might have found my AP and the dose to make life bearable. I’m on 10 mg olanzapine daily besides my AD.
You sound literally as a “brainy” person I guess you must have studied anatomy or neurology?
Joke aside - most of the recent research I have been reading tends to support the fact that AP’s support neurogenesis. I think, like @columbus and @jukebox says, the important thing is to steer out of psychosis and depression, since those symptoms degenerate the brain.
Yeah. Heh. I don’t even remember what I wrote. I was using the technical terminology in the article to try to condense in a single paragraph. Try to make some sense of it. Most of this high-level research is beyond my comprehension ability.
There was the part, though, that mentioned something about 28 days after taking an AP and experiencing neurogenesis. That actually happened to me after my first month taking Geodon daily. That was a great feeling that only lasted up to 24 hours. I’m definitely telling my pdoc about it whenever my next appointment is. That should be interesting.
I think that the atypical antipsychotics are even more neuroprotective than the older because they to a lesser degree bind to the dopamine receptors and to a greater degree bind to serotoninreceptors.
But last but not least the most important thing is to swallow the pills every day.
The previous paradigm in which pharmacologic therapies exert their efficacy primarily on neurochemical pathways is evolving toward a model in which neurotransmitter actions trigger various neuroplasticity cascades to rebuild the neural pathways ravaged by recurrent episodes of psychosis or depression.
Personally I always thought using heavier APs in the initial phase of schizophrenia could be beneficial as the quicker you can correct some of these imbalances then the more damage you limit. I thought interesting to hear that quetiapine, Olanzapine, risperidone cause BDNF/NGF upregulation. Also this is relevant to exercise.
I don’t even think it is necessarily FGA vs SGA as category. Obviously SGAs have benefits, however each of these medications is different and will have unique pharmacology effects. In reality some of these medications have to be better then others. These kind of things aren’t teased out in short term trials for example effects on BDNF/NGF could potentially have long term effects. Wish knew the answer to this for all of APs in heads up vs trials and then meta analyses.
@Bowens
Psychosis is brain damage is a general statement and not necessarily related to brain age. Each episode of psychosis and or relapse/hospitalisation decreases your chances of making a functional recovery. If anything psychosis is damaging in that it impairs your ability to function in society and interact with the environment. Brain damage doesn’t necessarily need to be categorised as cognitive function e.g. ability to read or solve math problems. It can also simply brain damage to social function. Any determential event which change the biological function of the organisms and decreases the total fitness of that organisms can be conceptualise as damage to it. Clearly these are happening within the brain I don’t think it is debatable whether psychosis is brain damage or not.
It is semantics. However the reason that your not hearing this information coming for doctors is that they actively telling you to stay on medication specifically to prevent relapse even in the absence of psychotic symptoms. It is not necessarily helpful to the patient to term things in this way. The incidence of disability in schizophrenia is apparent. What is causing the disability is damage that is in the brain. Each episode of psychosis make you worse. It might plateau eventually after a number of episodes but general rules and logic apply. Since we don’t know the cause of schizophrenia it is hard to say this is what exactly the brain damage is, but since it is also clear where it is happening (in the brain). I feel it is a semantic argument and presumptive but entirely correct statement to say psychosis is brain damage. The instance where it is really helpful to communicate this message in ultra high risk individuals of first episode psychosis, as both clinicians and psychotic patients already have their own nuanced understanding of this even if they don’t use this exact terminology. Still it remains true in it’s entirety.
I have to disagree. The information is indeed conflicting and unreliable, as I stated. No one knows if psychosis causes brain damage. And certainly not if its permanent. Prognosis is not the same as brain damage.
Thanks a lot @Iris_Crypts for your very informative answer. I guess all stressors affect the brain, and I can’t find anything more stressful than a psychosis.
Interesting, okay I’ll take it on that there is no definitive answer yet. Schizophrenia is normally categorised as development not neurodegenerative. Due to the late onset and multifactorial causes ultra high risk individuals aren’t necessarily destined to develop sz. Trauma and environmental factors play a role. Schizophrenia is clearly a multifactorial disease which is in the brain. People with schizophrenia simply put have damaged brains, this is the disability. The ability to make full recovery in schizophrenia is pretty damning. This not true of first episode psychosis but is true of schizophrenia. Schizophrenia can be conceptualised as a form of multiple episode psychosis that is ongoing. Often what initiates a couple of episodes of psychosis then develops into schizophrenia.
Given enough time a cure will be found for schizophrenia, likey not in our life time though. Semantically to me brain damage doesn’t need to be permanent to qualify as such, just enduring and not self correcting.
Schizophrenia is brain damage. Okay yeah it is presumtive and getting ahead of yourself to say psychosis is brain damage but it’s a position I hold. I would personally be suprised to see this position will be disproven in time. Maybe it’s not popular terminology though.
@Bowen Here is an open question, do you think each new and additional episode of psychosis in people already diganosed with schizophrenia could be classified as a brain damaging event?
I don’t think there is a definitive answer at this time. I have been looking at this stuff for years now. I have had beliefs on opposing sides of various arguments about brain damage, brain tissue loss, whether its permanent, whether aps protect the brain or harm it or maybe both(protect from psychosis damage but cause its own damage), etc, etc., and after a long time of going back and forth and reading one conflicting study after another, the only conclusion that I can come to at the current time is that there is no definitive answer yet.
If you look long enough at this stuff, your eyes begin to cross and your brain begins to melt. lol.