Reaching cells

BJPsych Editorial: Questioning the ‘neuroprotective’ hypothesis: Does drug treatment prevent brain damage in early psychosis or schizophrenia? By Joanna Moncrieff.
http://bjp.rcpsych.org/content/198/2/85.full

Reaching Cells, reply by Dr Peter J. Gordon, 9 February 2011: http://bjp.rcpsych.org/content/198/2/85/reply

As an old age psychiatrist, you may not be surprised to know that neuroprotection is a matter that I willingly reconsider in light of advancing science. However I currently share Dr Moncrieff’s reading of the evidence: that it is premature to advocate that antipsychotic medications are neuroprotective.[1] If this is indeed so, science must prove it, before it becomes rationale for intervention.

Like Dr Moncrieff, I do not argue against the appropriate use of antipsychotic medications, for so used they are our best treatment of such suffering. However, like aspirin[2], breast-feeding and rather many more recent examples under media focus, might medical science be adding to confusion by offering wisdom before supporting evidence is established? We should consider here that in March 2004, the Committee for Safety of Medicine advocated that risperidone and olanzapine, should not be used to treat psychotic symptoms in older patients with dementia as review had found that they caused a three-fold increase in the risk of stroke.[3]

Dr Moncrieff is also surely correct to raise the far from invisible spectre of tardive dyskinesia. As for Lithium, well it may be neurotrophic[4], and it is certainly a most effective mood stabiliser, but we must not forget that it is also potently nephrotic. As an old-age psychiatrist, I am very familiar with having to stop Lithium due to its effects on the kidney. It is anecdotal I know, but I have had many patients treated with lithium since early adulthood who have gone on to develop dementia.

Perhaps others reading this Editorial will have turned their thoughts to antidepressants and the evidence that they are potentially neuroprotective[5]? It was back in 2004 that Professor Reid of Aberdeen University published his paper New Cells, New Connections[6], revealing the relationship between stress and neurogenesis in the hippocampus. Perhaps I am alone, but I am bemused why such thoughtful research has not been made more of? Not least in that it offers a potential explanation of how one’s ‘early social landscape’ (formative relations and stresses) might account for later recurrent depression. Reid’s research here seems highly intuitive and pulls the swingometer back to the middle from the extremity of today’s neurodeterminism.

Having said all this, I am myself cynical that antidepressants are neuroprotective, even though some studies are now suggesting they can decrease both Alzheimer pathology and reverse memory impairment.[7] As many of such studies are based on rats administered paroxetine, perhaps we should wait a little before offering antidepressants as ‘Parr’s life pills.[8]’ Though at least I should be okay, as my hippocampus must be bursting with new neurons and considering such I can be confident that all I say here has the backing of brain like Einstein.

I shall not finish on that cynical note, just a cautionary one. Let our cells not over-reach in scientific conclusion until both good research, and time, reveal the whole story. Neuroprotection may be a truth, but surely science must prove such, before prescribing such an ‘optimiser.’ [9]

Parr's-Life-Pills


[1] Moncrieff, J; Questioning the ‘neuroprotective’ hypothesis: does drug treatment prevent brain damage in early psychosis or schizophrenia? The British Journal of Psychiatry (2011) 198: 85-87.

[2] Barnett, H; Burrill, P; Iheanacho, I: Change Page: Don’t use aspirin for primary prevention of cardiovascular disease BMJ 340 (Published 21 April 2010)

[3] Duff, G; Committe onSafety of Medicines; Atypical Antipsychotics and Stroke; 9th March 2004

[4] Zhu, Z; Wang, Q; Han, B; William, C: Neuroprotective effect and cognitive outcome of chronic lithium on traumatic brain injury in mice; Brain Research Bulletin, Volume 83, Issue 5, 30 October 2010, Pages 272-277

[5] Lloyd, A; Ferrier,N.I; Barber,R; Gholkar,A; Young,A.H; O’Brien,J: Hippocampal volume change in depression: late- and early-onset illness compared. The British Journal of Psychiatry, Jun 2004; 184: 488 – 495.

[6] Reid, I.C; Stewart, C.A: Brain Plasticity and Antidepressant Treatments: New Cells, New Connections. Neurotoxicity Research, 2004, VOL. 6(6). pp. 483-491

[7] Bales, K.R; Paroxetine administration decreases AD-like pathology and reverses memory impairments in a transgenic model of Alzheimer disease. Experimental neurology 2007 (2007) 1-3

[8] A corner of history: Preventive Medicine, Volume 1, Issue 4, December 1972, Pages 565-570

[9] Brain Profiling Group: Damian, M; Kreis, M; Krumm, B; Hentschel, F Optimized neuropsychological procedures at different stages of dementia diagnostics. Journal of the Neurological Sciences , 229-230 , 95-101. (2005).

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