The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer's disease.
Dis Model Mech
; 7(4): 445-58, 2014 Apr.
Article
en En
| MEDLINE
| ID: mdl-24574361
ABSTRACT
Circadian behavioural deficits, including sleep irregularity and restlessness in the evening, are a distressing early feature of Alzheimer's disease (AD). We have investigated these phenomena by studying the circadian behaviour of transgenic Drosophila expressing the amyloid beta peptide (Aß). We find that Aß expression results in an age-related loss of circadian behavioural rhythms despite ongoing normal molecular oscillations in the central clock neurons. Even in the absence of any behavioural correlate, the synchronised activity of the central clock remains protective, prolonging lifespan, in Aß flies just as it does in control flies. Confocal microscopy and bioluminescence measurements point to processes downstream of the molecular clock as the main site of Aß toxicity. In addition, there seems to be significant non-cell-autonomous Aß toxicity resulting in morphological and probably functional signalling deficits in central clock neurons.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Conducta
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Ritmo Circadiano
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Modelos Animales de Enfermedad
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Drosophila melanogaster
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Relojes Circadianos
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Enfermedad de Alzheimer
Límite:
Animals
Idioma:
En
Revista:
Dis Model Mech
Asunto de la revista:
MEDICINA
Año:
2014
Tipo del documento:
Article
País de afiliación:
Reino Unido