INVESTIGADORES
OTERO-LOSADA Matilde Estela
congresos y reuniones científicas
Título:
INTRINSIC (OLFACTORY) AND EXTRINSIC (VERBAL) MEMORY IN EARLY STAGES OF!!ALZHEIMER'S DISEASE
Autor/es:
OTERO-LOSADA, M.
Lugar:
Sorrento
Reunión:
Congreso; 7th International Conference on Alzheimer’s Disease and Parkinson’s Disease; 2005
Resumen:
Intrinsic (olfactory) and extrinsic (verbal) memory in early stages of Alzheimer’s disease. The neuroanatomical and neurochemical basis for disosmias are uncertain while there is an abundance of preclinical and clinical data linking olfaction with acetylcholine. This study aimed to evaluate peripheral and central olfaction early after clinical diagnosis of Alzheimer’s Disease (AD). Subjects (two age/ sex-matched groups, medication free): AD (68±8 yr, n=11), C (healthy controls) (66±12 yr, n=11). Methods: I. Olfactory detection threshold using n-1-butanol (paired comparison, forced choice) to evaluate peripheral function. II. Smell Identification (UPSIT, 40 microencapsulated complex odors, forced multiple choice) as an indicator of central odor processing using verbal (explicit) memory. III. Odor-odor Recognition-Identification (pure stimuli, forced mutiple choice), which results from central odor processing using non-verbal (implicit) memory. Statistical analysis: ANOVA (one-way). SPSSTM 10.0. Butanol threshold quantification showed no differences between the two groups (12% increase) [F (4.05; 1; 21), p<0.057, N.S.] while UPSIT procedure revealed lower performance in AD than in C (28% decrease of right answers) [F (6.72; 1; 21), p<0.017]. Both AD and C were indistinguishable according to non-verbal identification scores. It must be noticed that a small number of subjects were studied. These findings suggest that exclusive (own) memory subcircuits, fairly resistant to initial neurodegenerative damage, might subserve olfactory memory preservation while general memory circuits are already damaged (explicit memory deficit). Previous research indicates that such olfactory subcircuits would be affected by the widespread neuronal alteration at later stages of the disease. Our results appear to point to a central (not peripheral) ethiological factor in the onset of AD. Key: olfaction; Alzheimer’s; memory; thresholds