Chronic nicotine treatment reduces β‐amyloidosis in the brain of a mouse model of Alzheimer's disease (APPsw)

Alzheimer's disease neuropathology is characterised by β‐amyloid plaques and neurofibrillary tangles. Inhibition of β‐amyloid accumulation may be essential for effective therapy in Alzheimer's disease. In this study we have treated transgenic mice carrying the Swedish mutation of human amy...

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Veröffentlicht in:	Journal of neurochemistry 2002-05, Vol.81 (3), p.655-658
Hauptverfasser:	Nordberg, Agneta, Hellström‐Lindahl, Ewa, Lee, Mandy, Johnson, Mary, Mousavi, Malahat, Hall, Ros, Perry, Elaine, Bednar, Ivan, Court, Jennifer
Format:	Artikel
Sprache:	eng
Schlagworte:	Administration, Oral Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - analysis Amyloid beta-Peptides - biosynthesis amyloid β peptide Animals APPsw transgenic mice Astrocytes - metabolism Astrocytes - pathology Biological and medical sciences Brain Chemistry Cell Count Cerebral Cortex - drug effects Cerebral Cortex - metabolism Cerebral Cortex - pathology Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Disease Progression Drug Administration Schedule Female Glial Fibrillary Acidic Protein - biosynthesis Hippocampus - chemistry Humans Immunohistochemistry Male Medical sciences Medicin och hälsovetenskap Mice Mice, Transgenic Neurology nicotine Nicotine - administration & dosage nicotinic receptors Olfactory Pathways - chemistry Peptide Fragments - analysis Peptide Fragments - biosynthesis Plaque, Amyloid - drug effects Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Sex Factors Treatment Outcome
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Zusammenfassung:	Alzheimer's disease neuropathology is characterised by β‐amyloid plaques and neurofibrillary tangles. Inhibition of β‐amyloid accumulation may be essential for effective therapy in Alzheimer's disease. In this study we have treated transgenic mice carrying the Swedish mutation of human amyloid precursor protein [Tg(Hu.APP695.K670N‐M671L)2576], which develop brain β‐amyloid deposits, with nicotine in drinking fluid (200 µg/mL) from 9–14.5 months of age (5.5 months). A significant reduction in amyloid β peptide 1–42 positive plaques by more than 80% (p
ISSN:	0022-3042 1471-4159
DOI:	10.1046/j.1471-4159.2002.00874.x