They set out to study what connection there might be in the status of brain hippocampal function in depression.
To do that the team examined the level of new hippocampal cell activity in samples taken post mortem from brains that had been kept in a 'bank' store from three different kinds of people: those normal, those with depression, those with schizophrenia.
Without direct successful repetition of Reif et al it has been left for indirect corroboration from subsequent independent studies of memory status in schizophrenia.
No studies have refuted it. [ The studies were not challenging Reif et al ; their independent findings give predictive credence to Reif e al ]
The older the age at the onset of illness , the better is the useful practice already stored away, accumulated experience in personal, domestic, social, interests, occupational experience, that can be drawn upon in daily living.
Competence then is usually sufficient for a level of recovery.
Girls and young women on the whole have a better store of experience of domestic skills , are more verbally competent [ dare I say ! ] and thereby may have better outcomes after the illness arrives.
Delusional interference does not reach into the store held before the illness. ]
Schizophrenia is an illness of brain function. . An illness that affects the continual proliferation and use of memory cells.
It is not brain damage - as the memory cells are damaged in Alzheimers. Alzheimer's memory failure progresses as memory cells die off
In schizophrenia, there is a one off lessening of functioning in the proliferation of new stem cell derived memory cells within the hippocampal area of the brain, at the age of the onset of the illness
The level of intelligence is not reduced.
A critical brain tool - a Working Memory span - depends upon the proliferation and provision of enough of new cells by the dentate gyrus in the hippocampus area of the brain.
This is the critical area: reduced new cells = reduced working memory.
Those with reduced working memory can't cover all the background that is needed to be accessed. So what is presented is approximate, incomplete. What previously brought together enough
information from experience to deal with work-a-day matters is less able after theage of onset of the illness.
Insight depends upon recall, recollection of past experience and behaviour.
Hippocampal new memory cells are necessary for the recall of personal illness behaviour. It is clearly not recalled if at all. Somebody or something has done what has happened to me.
Working memory capacity is a better measure of 'intellectual' practical ability than IQ.
Working memory [ WM ] refers to
the short-term storage of enough information, drawn together in the service of the actively doing something, or thinking something through.
Working memory capacity [ WMC ] is the amount of information that can be carried and called to mind when putting one's mind to work. For example keeping up with the meaning of changes in a conversation. There is not enough capacity to hold in mind whatever went before that is relevant to your present situation, there to guide what ever you are going to do soon, or might need to do later on. You lose your way.
Recognising this is the basis of how to 'behave' with those with some level of this illness. Loss of working memory capacity from now on - not loss of intelligence - has to be taken into account when in coversation, when recovery and rehabilitation programmes are proposed to individual sufferers and to their carers.
What you are able to get from memory store at any one time is reduced. Recovery starts in a simplified environment with a shorter practice span,with plenty of unpressured time.
It is harder for participants to keep out distraction; 'noise' ... whatever stuff is going on around outside, grabs attention.
It is harder to complete a goal directed job at the same rate as before, especially if there is any pressure of time upon doing it.
Damaged cells as in Alzheimer's cannot recover themselves.
There are recoveries from schizophrenia, more often when the illness arrives later, probably when the personality before the illness was more outgoing and sociable - had gained more social experience - the extravert people rather than the quieter introvert kind of people.
The older the age of onset of the illness, the more social experience has been acquired.
Stem cell research is actively being pursued with experimental success.
Human stem cell when transplanted into a mouse hippocampus has taken up working there.
I am angry that the Research Community do not consider it their duty to replicate - or refute - the findings in the Reif study. It is seven years ago now. I think it disgraceful that the Established Psychiatric Community are not demanding the same.
In my mind that is an abuse of power. Power to deny information of value to the helpless, is as much an abuse of power as is exercising the power to corrupt..
If these people lived with or were affected by someone who has schizophrenia they would push a campaign to see if Reif et al finding could be a directly confirmed fact.
The public and carers, bewildered by the lack of explanation for the behaviour change in their family member,
will not understand how those in the Research and Health establishment, do not pursue this finding, are able to disregard and dismiss this possible opening to a better understanding of it.
I am not a lone crank ... DeCarolis ...[ " Caution is advised in the interpretation
of Reif et al because a decrease in Ki-67-expressing cells is not an index of overall
as not all dividing cells become neurons .
[ Ed:- but most do go on to neurons]
Even so, the links between hippocampal neurogenesis and schizophrenia are promising enough to inspire the proposition that an immature dentate gyrus, as might result from decreased neurogenesis,
is a novel endophenotype of psychiatric disorders like schizophrenia
thorough examination of human post-mortem samples is also desperately needed to better
understand human neurogenesis and how it is similar to, and distinct from, rodent neurogenesis
The fault that for me brings on schizophrenia is this fall in hippocampal stem cell proliferation; a once only drop in continually available new memory cells [ hippocampal neurogenesis ] in the brain, that persists: to keep up with changes to living demands, continually formed new memory cells are necessary .
Less new memory cells leads to less memory at work as before the illness. The decisive change.
That is why they do not 'move on', but stick at the level they had reached before the illness struck.
The hippocampus engages with many other brain sites. It is as active in sleep as it is awake.
Sleep is now believed to be the time when what has been acquired in memory during the day gets sorted out and put where it has value.
Together, the hippocampus with the executive frontal brain cortex decide whatever from what is going on outside should receive attention, be of significance, be allowed in; the rest to be not salient and ignored.Many people with active schizophrenia feel that 'outside' presses it's attention, distracting other matters that should be given priorit.
Less hippocampal memory cells means that what should have been set aside as irrelevant, now is allowed in as emotionally important in some way, that has to be given a story to reconcile it with the rest of stored away experience. '.
So where is it to go to get the importance it was given during the daytime intake. Where is to be assigned a salient network.?
There are two kinds of sleep .
One proposal is that REM sleep deals with what the slow wave sleep has left over because it is unusually 'admitted'. The untidy emotional bits from the day's memories .
REM sleep is when rather frightening dreams can occur. Dreams which subject the dreamer .
Is REM sleep there to deal with the uncertain material that has got in - insignificant normally, but now given emotional weight, expicable in a delusional misinterpretation ?
Reduced hippocampal new memory cells at the start of the illness will lead to abnormalities in the way these tidying up sleep stages do their work.
Three changes happen AT THE SAME TIME with the start of schizophrenia that need an explanatory story for this timing
1. venricular enlargement
2. cognitive impairment - sufferers do not move on from what they already know.
3. The world seems noisier, seems to press harder upon the sufferer. Subsequently but within the same time frame a misbelief system arrives, and this delusional story of explanation persists, often worse because of 3.
There is a need to explain also how it is that sufferers manage to live in two worlds:
that of a undue sensitivity to what is going on around them, often leading to an irrefutable delusional account to explain it;
a continuing if fragile ability to manage attending to the usual living demands.
That ability is limited by whatever store of competence in living they had before the age when the illness arrived.
How is it that more or less efficacious medications are all dopamine blockers.
[ It estimated that only 3 percent of adherent patients would relapse in the first year, compared to an estimated 77 percent of patients who stop their medication, indicating that the risk of relapse is very low when these patients remain fully adherent to their antipsychotic medication ]
How would hippocampal neurogenesis failure at the age of onset of the illnss account for the changes that come after the illness, happening together, account for the key diagnostic elements of schizophrenia
How would accepting that help in the care of schizophrenia.
monthly*** New !!! Social worker - not a medically qualified psychiatrist - becomes the senior clinical [ Responsible Clinician ] community Tratment Order [ CTO ] lead figure in Norfolk and Suffolk Trust
Dunedin 1000 babies in the same year in the same town: a 95% follow up till aged thirty-eight.
3% developed schizophrenia over these forty years.
They had shown a falling off of cognitive performance ' intelligence' some around seven years before adolescence, when then there was a more substantial drop.
2012-2013 Figures:- In-patient Admissions .. .. Community Treatment Orders
Open letter to the reviewer of a big book listed in the October issue of the British Journal of Psychatry about 'Cognitive Impairment in Schizophrenia'.
The Government has reviewed the 2007 Mental Health Act and has made Recommendations
Quite often no beds in the whole of the country. That increases the burden on families receiving Home 'Treatment' , and the possibility of misjudging risk, and of dealing with it.
The people responsible for ensuring bed availablility are the local Clinical Commissioning Group, not the Trust providing that service, although CCG's behave as though they can leave that responsibility to the Delivering Trust.
It would be up to the Trust to appeal to the CCG for provision funding, saying they are not providing a legally obliged service. At present , surveys are finding an inadequate provision.
I hope a Charity or an individual will see and find grounds to go to Judicial Review about the failure to commission and provide.
*** New !!!
Carbon dating !!!
A quite different way of measuring the state of neurogenesis in the dentate gyrus of the hippocampus has emerged.
Clozapine [ Clozaril ]
How to behave towards people with schizophrenia