Reduced plasma leptin and elevated homocysteine (Hcy) are known to lead to increased β-amyloid (Aβ) production, besides being hallmarks of anorexia nervosa (AN) of the restrictive type. AN subjects display several neuropsychiatric manifestations, which may entail Aβ-mediated altered synaptic functions. The aim of this study consisted in assessing Aβ plasma levels in AN patients. Methods: A total of 24 adolescent female AN outpatients were recruited together with 12 age-comparable healthy controls. For each subject we assessed Aβ40 and leptin plasma levels, as well as APOE genotype. Hcy plasma levels were also determined in AN patients who underwent clinical characterization, including the Eating Disorder Inventory-3 (EDI-3), the Children's Depression Inventory (CDI) and the estimation of the speed of BMI loss (DPI, disease progression index). Results: Plasma Aβ40 levels were similar between patients and controls, while a marked reduction was observed for leptin (∼80%) in AN patients. Aβ40 plasma levels failed to correlate with leptin, while a linear correlation was present with Hcy (r = 0.50, p < 0.03). Examined clinical features were not related with Aβ40 plasma levels, with the only exception of the DPI (r = 0.47, p < 0.03). Conclusion: This exploratory study does not support a significant role for altered Aβ production in AN-associated dysfunctions. Further studies are required to clarify whether exceptions to this conclusion can be drawn for those patients expressing significantly elevated Hcy plasma levels or for those progressing more rapidly.

Conti, E., Nacinovich, R., Bomba, M., Raggi, M., Neri, F., Ferrarese, C., et al. (2015). Beta-amyloid plasma levels in adolescents with anorexia nervosa of the restrictive type. NEUROPSYCHOBIOLOGY, 71(3), 154-157 [10.1159/000381399].

Beta-amyloid plasma levels in adolescents with anorexia nervosa of the restrictive type

CONTI, ELISA
Primo
;
NACINOVICH, RENATA
Secondo
;
BOMBA, MONICA;NERI, FRANCESCA;FERRARESE, CARLO
Penultimo
;
TREMOLIZZO, LUCIO
Ultimo
2015

Abstract

Reduced plasma leptin and elevated homocysteine (Hcy) are known to lead to increased β-amyloid (Aβ) production, besides being hallmarks of anorexia nervosa (AN) of the restrictive type. AN subjects display several neuropsychiatric manifestations, which may entail Aβ-mediated altered synaptic functions. The aim of this study consisted in assessing Aβ plasma levels in AN patients. Methods: A total of 24 adolescent female AN outpatients were recruited together with 12 age-comparable healthy controls. For each subject we assessed Aβ40 and leptin plasma levels, as well as APOE genotype. Hcy plasma levels were also determined in AN patients who underwent clinical characterization, including the Eating Disorder Inventory-3 (EDI-3), the Children's Depression Inventory (CDI) and the estimation of the speed of BMI loss (DPI, disease progression index). Results: Plasma Aβ40 levels were similar between patients and controls, while a marked reduction was observed for leptin (∼80%) in AN patients. Aβ40 plasma levels failed to correlate with leptin, while a linear correlation was present with Hcy (r = 0.50, p < 0.03). Examined clinical features were not related with Aβ40 plasma levels, with the only exception of the DPI (r = 0.47, p < 0.03). Conclusion: This exploratory study does not support a significant role for altered Aβ production in AN-associated dysfunctions. Further studies are required to clarify whether exceptions to this conclusion can be drawn for those patients expressing significantly elevated Hcy plasma levels or for those progressing more rapidly.
Articolo in rivista - Articolo scientifico
Anorexia nervosa; Homocysteine; Plasma leptin; β-Amyloid;
Anorexia nervosa; Homocysteine; Plasma leptin; β-Amyloid; Psychiatry and Mental Health; Neuropsychology and Physiological Psychology; Biological Psychiatry
English
2015
71
3
154
157
reserved
Conti, E., Nacinovich, R., Bomba, M., Raggi, M., Neri, F., Ferrarese, C., et al. (2015). Beta-amyloid plasma levels in adolescents with anorexia nervosa of the restrictive type. NEUROPSYCHOBIOLOGY, 71(3), 154-157 [10.1159/000381399].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/91054
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