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                                       Details van artikel 4 van 23 gevonden artikelen
 
 
  Differential Expression of Interneuron Populations and Correlation with Amyloid-β Deposition in the Olfactory Cortex of an AβPP/PS1 Transgenic Mouse Model of Alzheimer's Disease
 
 
Titel: Differential Expression of Interneuron Populations and Correlation with Amyloid-β Deposition in the Olfactory Cortex of an AβPP/PS1 Transgenic Mouse Model of Alzheimer's Disease
Auteur: Saiz-Sanchez, Daniel
Ubeda-Bañon, Isabel
De la Rosa-Prieto, Carlos
Martinez-Marcos, Alino
Verschenen in: Journal of Alzheimer's disease
Paginering: Jaargang 31 (2012) nr. 1 pagina's 113-129
Jaar: 2012-04-27
Inhoud: Impaired olfaction is an early symptom of Alzheimer's disease (AD). Neuroanatomical changes underlying this deficit in the olfactory system are largely unknown. Cell neurodegeneration is known to involve, among others, somatostatin (SST)- and calcium-binding protein-positive cells. We report here quantitative analysis of temporal changes in the distribution of interneuron cell populations in the olfactory cortex of an AβPP/PS1 double-transgenic mouse model of AD and its correlation with amyloid-β pathology. To investigate early stages of pathology, the piriform and lateral entorhinal cortices were analyzed in groups of homozygous AβPP/PS1 and control animals at 2, 4, 6, and 8 months of age. There was a significant increase in brain levels of aggregated amyloid-β peptide with age, accompanied by an early and marked fall in numbers of SST- and calretinin-positive interneurons; a later and less pronounced decrease in levels of calbindin- and parvalbumin-positive cells was also observed. In addition, double-labeling experiments indicated high levels of co-localization of SST-positive cells with amyloid-β expression in olfactory areas. These observations argue that SST-positive cells are vulnerable to amyloid-β neuropathy in the olfactory cortex during the early stages of AD. These data may cast light on the neural basis of hyposmia associated with this disorder and on the mechanisms of cell vulnerability to neurodegeneration.
Uitgever: IOS Press
Bronbestand: Elektronische Wetenschappelijke Tijdschriften
 
 

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