title: State-dependent alterations in cerebrospinal fluid Aβ42 levels in cognitively intact elderly with late-life major depression.
abstract: Depression has been linked to Alzheimer's disease as either an increased risk factor for its development or as a prodromal symptom. The neurobiological basis for such an association, however, remains poorly understood. Numerous studies have examined whether changes in amyloid beta (Aβ) metabolism, which are implicated in the pathogenesis of Alzheimer's disease, are also found in depression. In this paper, we investigated the relationship between depressive symptoms and cerebrospinal fluid (CSF) Aβ indices in otherwise healthy, cognitively normal elderly with late-life major depression (LLMD) and controls using a longitudinal approach, which is a novel contribution toward the literature. Significantly lower levels of CSF Aβ42 were observed in the LLMD group at baseline and were associated with more severe depressive symptoms. During longitudinal follow-up, the depressed group remained cognitively unchanged, but was significantly less depressed than at baseline. A greater improvement in depressive symptoms was associated with increases in CSF Aβ42 levels in both groups. Increases in CSF Aβ42 and Aβ40 were also associated with increased CSF total-tau levels. Our results suggest that LLMD may be associated with state-dependent effects of CSF Aβ42 levels. Future studies should determine whether the association reflects state-dependent changes in neuronal activity and/or brain amyloid burden in depression.
authors: aGeriatric Psychiatry Division, Nathan S. Kline Institute, Orangeburg Departments of bPsychiatry cSteve and Alexandra Cohen Veterans Center dNeurology, Pathology and Psychiatry eCenter for Brain Health, NYU Langone Medical Center fProgram in Behavioral and Cognitive Neuroscience, The Graduate Center of the City University of New York, New York City, New York, USA gSchool of Natural Sciences and Psychology, Liverpool John Moores University, Liverpool hDepartment of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK iClinical Neurochemistry Laboratory, Sahlgrenska University Hospital jDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
authors: Nunzio
authors: N
authors: Pomara
authors: Davide
authors: D
authors: Bruno
authors: Ricardo S
authors: RS
authors: Osorio
authors: Chelsea
authors: C
authors: Reichert
authors: Jay
authors: J
authors: Nierenberg
authors: Antero S
authors: AS
authors: Sarreal
authors: Raymundo T
authors: RT
authors: Hernando
authors: Charles R
authors: CR
authors: Marmar
authors: Thomas
authors: T
authors: Wisniewski
authors: Henrik
authors: H
authors: Zetterberg
authors: Kaj
authors: K
authors: Blennow
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000134:cerebrospinal fluid*; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid*; D016022:Case-Control Studies; D003865:Major Depressive Disorder / Q000134:cerebrospinal fluid*; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000134:cerebrospinal fluid*; D011569:Psychiatric Status Rating Scales; D016875:tau Proteins / Q000134:cerebrospinal fluid
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42); D016875:tau Proteins