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The deposition of amyloid beta peptide (A beta) is an early and critical aspect of Alzheimer's disease. A beta is formed by the cleavage of amyloid precursor protein (APP). Studies of familial forms of Alzheimer's disease indicate that elevated secretion of A beta, particularly A beta(1-42), is likely to be an etiologic agent in the disease. A beta(1-42) is(More)
Neurotensin (NT) is a tridecapeptide neurotransmitter in the central nervous system. It has been implicated in the therapeutic effects of neuroleptics. Central activity of NT can only be demonstrated by direct injection into the brain, since it is readily degraded by peptidases in the periphery. We have developed many NT(8-13) analogs that are resistant to(More)
NT69L, a neurotensin analog that crosses the blood-brain barrier, reduces body temperature, reverses apomorphine-induced climbing, haloperidol-induced catalepsy, and D-amphetamine- and cocaine-induced locomotor activity in rats. In this study we tested the development of tolerance to these effects of NT69L in rats. The blockade of apomorphine-induced(More)
This review will be an update, focusing on the central nervous system (CNS) roles of the neurotransmitter, neurotensin. We will provide a summary of current knowledge about neurotensin, why it is an important peptide to study, and where the field is heading. Special emphasis is placed on the development of neurotensin analogs, which has been a major effort(More)
To determine the effectiveness of peptide nucleic acids (PNAs) in vivo, we designed and synthesized PNAs antisense to the mu receptor, the molecular target of morphine for inducing antinociception. Responsiveness of rats to morphine and the levels of mu receptor expression after treatment was measured. We delivered intraperitoneal injections of antisense(More)
The depositing in brain of amyloid beta peptide (Abeta), which is formed by the cleavage of amyloid precursor protein (APP), is likely an etiologic factor in Alzheimer's disease (AD). Of the different forms of Abeta, Abeta(1-42) causes fibril formation and increases aggregation at elevated levels, which can lead to neuronal death. It is hypothesized that if(More)
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