Retinal changes in the Tg-SwDI mouse model of Alzheimer’s disease
Autor: | Thomas van Groen, Mark Bolding, Christianne E. Strang, Fred G. Oliveira-Souza, Alexis E. Lambert, Marci L DeRamus |
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Rok vydání: | 2017 |
Předmět: |
Aging
Pathology medicine.medical_specialty Green Fluorescent Proteins Vision Disorders Mice Transgenic Biology Retina Article Presenilin Choline O-Acetyltransferase Amyloid beta-Protein Precursor Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation Alzheimer Disease Cerebellum Glial Fibrillary Acidic Protein Presenilin-1 medicine Animals Humans Receptors Cholinergic Visual Pathways RNA Messenger Neurotransmitter Glial fibrillary acidic protein General Neuroscience Retinal medicine.disease Disease Models Animal medicine.anatomical_structure Gene Expression Regulation chemistry Mutation 030221 ophthalmology & optometry biology.protein Cholinergic sense organs Alzheimer's disease 030217 neurology & neurosurgery |
Zdroj: | Neuroscience. 354:43-53 |
ISSN: | 0306-4522 |
Popis: | Alzheimer's disease (AD), a debilitating neurodegenerative illness, is characterized by neuronal cell loss, mental deficits, and abnormalities in several neurotransmitter and protein systems. AD is also associated with visual disturbances, but their causes remain unidentified. We hypothesize that the visual disturbances stem from retinal changes, particularly changes in the retinal cholinergic system, and that the etiology in the retina parallels the etiology in the rest of the brain. To test our hypothesis, quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC) were employed to assess changes in acetylcholine receptor (AChR) gene expression, number of retinal cells, and astrocytic gliosis in the Transgenic Swedish, Dutch and Iowa (Tg-SwDI) mouse model as compared to age-matched wild-type (WT). We observed that Tg-SwDI mice showed an initial upregulation of AChR gene expression early on (young adults and middle-aged adults), but a downregulation later on (old adults). Furthermore, transgenic animals displayed significant cell loss in the photoreceptor layer and inner retina of the young adult animals, as well as specific cholinergic cell loss, and increased astrocytic gliosis in the middle-aged adult and old adult groups. Our results suggest that the changes observed in AD cerebrum are also present in the retina and may be, at least in part, responsible for the visual deficits associated with the disease. |
Databáze: | OpenAIRE |
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