Abstract: A transgenic mouse whose genome comprises a DNA sequence encoding the carboxy-terminal 100 amino acids of the human .beta.-amyloid precursor protein C-100 APP) inserted into exon I of the neurofilament gene such that all or part of exon I has been deleted is disclosed. Expression of the nucleic acid sequence is under the control of neurofilament L-gene regulatory region. The mouse as a result of the expression exhibits a brain morphology of an increased amyloid accumulation, and increase in reactive astrocytes, an increased microglial activation and a decreased number of neurons, and also exhibits spatial memory impairment.

Abstract: Light-emitting compounds of the formula: ##STR1## where R.sub.1 is a light-emitting moiety and R.sub.2 is a somatostatin-based peptide featuring a first amino acid sequence -Phe-Phe-Trp-Lys-Thr- or (SEQ ID NO:1) or -Phe-Phe-D-Trp-Lys-Thr-. The peptide is linked at a first amino acid position to (C-X), and the light-emitting compound exhibits substantial biological activity in the presence of a receptor having affinity for somatostatin-based peptides.

Abstract: Light-emitting compounds of the formula: ##STR1## where R.sub.1 is a light-emitting moiety and R.sub.2 is a somatostatin-based peptide featuring a first amino acid sequence --Phe--Phe--Trp--Lys--Thr-- (SEQ ID NO:1) or --Phe--Phe--D--Trp--Lys--Thr--. The peptide is linked at a first amino acid position to (C--X), and the light-emitting compound exhibits substantial biological activity in the presence of a receptor having affinity for somatostatin-based peptides.