F. Frank LeFever wrote:
> Maybe instead of reading more and
> more finer and finer detail about LTP, why not read v-e-r-y
> just ONE good GENERAL review for the LAY reader, then sit back and try
>> to digest it and understand it.
Wow, Frank - this seems unusually harsh coming from you.... it seems
to me like Hemidactylus has put in a good faith effort to check out some
relevant literature before posting his ideas/questions.
> You wonder about the "possible relationships of Alzheimer's disease
> 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
> 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
> of Alzheimer's, but this is far from certain unless one simply
> (carelessly) equates LTP and memory.
Alzheimer's disease is characterized by progressive dementia and a
characteristic neuropathology - the appearance of large numbers of
senile placques and neurofibrillary tangles. Indeed, a diagnosis of
Alzheimer's is not definitive until a neuropathologist verifies the
prescence of these. Because of this characteristic pathology (as well
as the frequent cortical atrophy), it is usually assumed that the
symptoms of AD result from the DEATH of cortical neurons. Those
investigating LTP in transgenic AD models are addressing the alternative
possibility that the dementia may not be due strictly to loss of
neurons, but rather/also from dysfunction of neurons. To my knowledge,
there has been evidence (suggestive, not conclusive) that hippocampal
LTP is impaired in transgenic mice models of familial AD, and
furthermore that this reduced LTP occurs prior to the appearance of any
neuropathological changes. Paul Chapman (in Wales) has been working on
this I believe - I was unaware of the Nalbantoglu et al paper (thanks).
>>> 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
> >of Alzheimer's disease and LTP, but on a Medline search I found
> >articles, one of which I had immediate access to. The article
> (Nalbantoglu et
> >al, 1997) discusses research using transgenic mice with a segment of
> >precursor protein (APP) incorporated into their genome. These mice
> >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
> to get
> >a better grasp of this issue.
> >Among the many studies I managed to find, a review by Bliss and
> >(1993) seems to have the best overview of LTP and its complexity. The
> >studies I've obtained are issue specific.
> >Bliss TVP and Collingridge GL. 1993. A synaptic model of memory:
> >potentiation in the hippocampus. Nature (361): 31-9
> >Nalbantoglu J, Tirado-Santiago G, Lahsaini A, et al. 1997. Impaired
> >and LTP in mice expressing the carboxy terminus of the Alzheimer
> >precursor protein. Nature (387): 500-5
> >Scott Chase (note followups at anthym at webtv.net)
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