In bionet.neuroscience John H. <johnhkm at netsprintXXXX.net.au> wrote:
> <dag.stenberg at helsinki.nospam.fi> wrote in message
> > The hippocampal regeneration result may have very little or nothing
> > to do with depression symptoms.
> Dag strikes again.
> Cortisol levels during human aging predict hippocampal atrophy and memory
> nature neuroscience . volume 1 no 1 . may 1998
Pages 69-73, by Lupien &al.
> brief extract:
> "Adrenalectomy at mid-life, with low-level glucocorticoid replacement,
> attenuates hippocampal degeneration and cogni-tive decline in rats 5 ,
> suggesting that elevated glucocorticoid lev-els directly contribute to the
> development of cognitive impairments. Together, these results strongly
> suggest that gluco-corticoid elevation partly accounts for individual
> differences in age-related hippocampal damage and memory defects in
Yes, cognitive impairment and memory defects.
> The glucocorticoid replacement is probably to maintain basal levels as this
> enhances cognition. A little stress goes a long way perhaps, too much and
> you might become the village idiot.
You apparently refer to the difference between acute and chronic
exposure to stress/glucocorticoids.
> Depression - stress - ...
I cannot find a single reference to depression in the article by Lupien
&al. Are you speaking for yourself in the following?
> My bet is that hippocampal atrophy is caused by the depressive symptoms
> which explains why depression lowers memory function.
My point was that the relationship between depression and hippocampal
atrophy is unclear, and need not be specific to anything in depression.
There is at least this study, though:
Sheline YI, Sanghavi M, Mintun MA, Gado MH
J Neurosci 1999 Jun 15;19(12):5034-43
Depression duration but not age predicts hippocampal volume loss in
medically healthy women with recurrent major depression.
This study takes advantage of continuing advances in the precision of
magnetic resonance imaging (MRI) to quantify hippocampal
volumes in a series of human subjects with a history of depression
compared with controls. We sought to test the hypothesis that
both age and duration of past depression would be inversely and
independently correlated with hippocampal volume. A sample of 24
women ranging in age from 23 to 86 years with a history of recurrent
major depression, but no medical comorbidity, and 24
case-matched controls underwent MRI scanning. Subjects with a history of
depression (post-depressed) had smaller hippocampal
volumes bilaterally than controls. Post-depressives also had smaller
amygdala core nuclei volumes, and these volumes correlated
with hippocampal volumes. In addition, post-depressives scored lower in
verbal memory, a neuropsychological measure of
hippocampal function, suggesting that the volume loss was related to an
aspect of cognitive functioning. In contrast, there was no
difference in overall brain size or general intellectual performance.
Contrary to our initial hypothesis, there was no significant
correlation between hippocampal volume and age in either post-depressive
or control subjects, whereas there was a significant
correlation with total lifetime duration of depression. This suggests
that repeated stress during recurrent depressive episodes may
result in cumulative hippocampal injury as reflected in volume loss.
Nothing is said about glucocorticoid load, so we are still only guessing,
aren't we? But the hypothesis is certainly nice.