Protection against developmental retardation in apolipoprotein E-deficient mice by a fatty neuropeptide: Implications for early treatment of Alzheimer's disease
✍ Scribed by Gozes, Illana ;Bachar, Michal ;Bardea, Amos ;Davidson, Ariane ;Rubinraut, Sarah ;Fridkin, Mati ;Giladi, Eli
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 152 KB
- Volume
- 33
- Category
- Article
- ISSN
- 0022-3034
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✦ Synopsis
Stearyl-Nle 17 -VIP (SNV) is a novel milestones, with peptide-treated animals developing agonist of vasoactive intestinal peptide (VIP) exhibas fast as control animals and exhibiting improved iting a 100-fold greater potency than the parent molecule and specificity for a receptor associated with neucognitive functions after cessation of peptide treatronal survival. Here, mice deficient in apolipoprotein ment. Specificity was demonstrated in that treatment E (ApoE), a molecule associated with the etiology of with a related peptide (PACAP), pituitary adenylate Alzheimer's disease, served as a model to investigate cyclase-activating peptide, produced only limited amethe developmental and protective effects of SNV. In lioration. As certain genotypes of ApoE increase the comparison to control animals, the deficient mice exprobability of Alzheimer's disease, early counseling hibited (a) reduced amounts of VIP messenger RNA; and preventive treatments may now offer an im-(b) decreased cholinergic activity (c) significant retarportant route for therapeutics design. ᭧ 1997 John dation in the acquisition of developmental milestones: