| Autor: |
Nyarko JNK; 1 Cell Signalling Laboratory, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan, Canada., Quartey MO; 1 Cell Signalling Laboratory, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan, Canada., Baker GB; 2 Department of Psychiatry, Neuroscience and Mental Health Institute, Neurochemical Research Unit, University of Alberta, Edmonton, Alberta, Canada., Mousseau DD; 1 Cell Signalling Laboratory, Department of Psychiatry, University of Saskatchewan, Saskatoon, Saskatchewan, Canada. |
| Abstrakt: |
The focus on the β-amyloid (Aβ) peptide in clinical Alzheimer disease (AD) as well as in animal models of AD has perhaps biased our understanding of what contributes to the heterogeneity in disease onset and progression. Part of this heterogeneity could reflect the various neuropsychiatric risk factors that present with common symptomatology and can predispose the brain to AD-like changes. One such risk factor is depression. Animal models, particularly mouse models carrying variants of AD-related gene(s), many of which lead to an accumulation of Aβ, suggest that a fundamental shift in depression-related monoaminergic systems (including serotonin and noradrenaline) is a strong indicator of the altered cellular function associated with the earlier(est) stages of AD-related pathology. These changes in monoaminergic neurochemistry could provide for relevant targets for intervention in clinical AD and/or could support a polypharmacy strategy, which might include the targeting of Aβ, in vulnerable populations. Future studies must also include female mice as well as male mice in animal model studies on the relationship between depression and AD. |
