long term potentiation

F. Frank LeFever flefever at ix.netcom.com
Tue Oct 13 20:25:47 EST 1998


Maybe I'm just misreading you, but it appears you are missing the
forest for the trees or putting the cart before the horse or doing
something equally as inappropriate.  Maybe instead of reading more and
more finer and finer detail about LTP, why not read v-e-r-y s-l-o-w-l-y
just ONE good GENERAL review for the LAY reader, then sit back and try
to digest it and understand it.

You wonder about the "possible relationships of Alzheimer's disease and
LTP", but it is not clear from what you write just what possible
relationships you imagine.

  LTP is a condition of enhanced synaptic efficiency lasting long after
the stimulation which initiates it, and as such has been suggested as
either a model for synaptic plasticity or actually a normal process
which underlies memory formation.  Conditions which impair LTP seem to
impair learning and long-term memory.  Accordingly, many pathologies
which involve impaired memory might be based on interference with
initiation or maintenance of LTP--but many others might not be.

  Thus, it seems unlikely that LTP causes Alzheimer's, or that
Alzheimer's causes LTP; conceivably impaired LTP underlies some aspects
of Alzheimer's, but this is far from certain unless one simply
(carelessly) equates LTP and memory.

I believe current thinking is in terms of mechanisms of cell
malfunction and/or death, most notoriously cholinergic nerve cells
(hence desperate efforts to boost cholinergic precursors or augment 
cholinergic activity via agonists or anti-antagonists, etc.)--but these
are only the first noticed and most widely studied.

Not too surprising if dead or dying cells cannot initiate or maintain
LTP.

HOWEVER, I suppose if one focuses on growth and maintenance rather than
memory formation, and if one could show that impaired LTP was the
leading edge of failing ggrowth and maintenance, well...

re APP: this has important normal roles in neural physiology, at least
in its soluble form--if I understand the theory correctly, it is a
problem in excretion (from the cell) of another APP fragment which
leads to amyloid deposits. (I don't think the transgenic mice had a
fragment of the protein in their genome; more likely their genome
included instructions for overproducing the problematic fragment)

F. Frank LeFever, Ph.D.
New York Neuropsychology Group





In <6vrhkq$8ac$1 at nnrp1.dejanews.com> Hemidactylus at my-dejanews.com
writes: 
>
>On my journey through the vast LTP literature in the library, I
managed to
>find some decent articles. I'm still not clear on the possible
relationships
>of Alzheimer's disease and LTP, but on a Medline search I found
several
>articles, one of which I had immediate access to. The article
(Nalbantoglu et
>al, 1997) discusses research using transgenic mice with a segment of
amyloid
>precursor protein (APP) incorporated into their genome. These mice had
LTP
>maintenance deficits. I wonder what inferences about the relation of
LTP and
>AD in humans can be made. I need to hunt down similar studies in order
to get
>a better grasp of this issue.
>
>Among the many studies I managed to find, a review by Bliss and
Collingridge
>(1993) seems to have the best overview of LTP and its complexity. The
other
>studies I've obtained are issue specific.
>
>refs:
>
>Bliss TVP and Collingridge GL. 1993. A synaptic model of memory:
long-term
>potentiation in the hippocampus. Nature (361): 31-9
>
>Nalbantoglu J, Tirado-Santiago G, Lahsaini A, et al. 1997. Impaired
learning
>and LTP in mice expressing the carboxy terminus of the Alzheimer
amyloid
>precursor protein. Nature (387): 500-5
>
>--
>Scott Chase (note followups at anthym at webtv.net)
>
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