| Autor: |
Xu W; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, New York, United States of America., Lopez-Guzman M; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America., Schoen C; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America., Fitzgerald S; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America., Lauer SL; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America., Nixon RA; Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Department of Psychiatry, New York University School of Medicine, New York, New York, United States of America; Department of Cell Biology, New York University School of Medicine, New York, New York, United States of America., Levy E; Center for Dementia Research, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Department of Psychiatry, New York University School of Medicine, New York, New York, United States of America; Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York, United States of America., Wilson DA; Emotional Brain Institute, Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, United States of America; Department of Child and Adolescent Psychiatry, New York University School of Medicine, New York, New York, United States of America; Department of Neuroscience and Physiology, New York University School of Medicine, New York, New York, United States of America. |
| Abstrakt: |
Alzheimer's disease is a neurodegenerative disorder that is the most common cause of dementia in the elderly today. One of the earliest reported signs of Alzheimer's disease is olfactory dysfunction, which may manifest in a variety of ways. The present study sought to address this issue by investigating odor coding in the anterior piriform cortex, the primary cortical region involved in higher order olfactory function, and how it relates to performance on olfactory behavioral tasks. An olfactory habituation task was performed on cohorts of transgenic and age-matched wild-type mice at 3, 6 and 12 months of age. These animals were then anesthetized and acute, single-unit electrophysiology was performed in the anterior piriform cortex. In addition, in a separate group of animals, a longitudinal odor discrimination task was conducted from 3-12 months of age. Results showed that while odor habituation was impaired at all ages, Tg2576 performed comparably to age-matched wild-type mice on the olfactory discrimination task. The behavioral data mirrored intact anterior piriform cortex single-unit odor responses and receptive fields in Tg2576, which were comparable to wild-type at all age groups. The present results suggest that odor processing in the olfactory cortex and basic odor discrimination is especially robust in the face of amyloid β precursor protein (AβPP) over-expression and advancing amyloid β (Aβ) pathology. Odor identification deficits known to emerge early in Alzheimer's disease progression, therefore, may reflect impairments in linking the odor percept to associated labels in cortical regions upstream of the primary olfactory pathway, rather than in the basic odor processing itself. |
