Journal of Alzheimers Disease & Parkinsonism
Open Access

Research Article

CSF and Brain Indices of Insulin Resistance, Oxidative Stress and Neuro-Inflammation in Early versus Late Alzheimer ' s Disease

Sarah Lee¹, Ming Tong¹, Steven Hang², Chetram Deochand³ and Suzanne de la Monte^4*

¹Department of Medicine, Rhode Island Hospital, Warren Alpert Medical School, Providence, RI, USA

²Department of Medicine, Warren Alpert Medical School, Providence, RI, USA

³Departments of Medicine, Rhode Island Hospital, Brown University, Providence, RI, USA

⁴Department of Medicine, Pathology (Neuropathology), Neurology and Neurosurgery, Rhode Island Hospital, Warren Alpert Medical School, Brown University, Providence, RI, USA

Corresponding Author:

Suzanne de la Monte
Pierre Galletti Research Building
Rhode Island Hospital, 55 Claverick Street
Room 419, Providence, RI 02903, USA
Tel: 401-444-7364
Fax: 401-444-2939
E-mail: Suzanne_DeLaMonte_MD@Brown.edu

Received date: September 21, 2013; Accepted date: October 24, 2013; Published date: October 31, 2013

Citation: Lee S, Tong M, Hang S, Deochand C, de la Monte S (2013) CSF and Brain Indices of Insulin Resistance, Oxidative Stress and Neuro-Inflammation in Early versus Late Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 3:128. doi: 10.4172/2161-0460.1000128

Copyright: © 2013 Lee S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Alzheimer’s disease (AD) is characterized by progressive impairments in cognitive and behavioral functions with deficits in learning, memory and executive reasoning. Growing evidence points toward brain insulin and insulin-like growth factor (IGF) resistance-mediated metabolic derangements ascritical etiologic factors in AD. This suggests that indices of insulin/IGF resistance and their consequences, i.e. oxidative stress, neuro-inflammation, and reduced neuronal plasticity, should be included in biomarker panels for AD. Herein, weexamine a range of metabolic, inflammatory, stress, and neuronal plasticity related proteins in early AD, late AD, and aged control postmortem brain, postmortem ventricular fluid (VF), and clinical cerebrospinal fluid (CSF) samples. In AD brain, VF, and CSF samples the trends with respect to alterations in metabolic, neurotrophin, and stress indices were similar, but for pro-inflammatory cytokines, the patterns were discordant. With the greater severities of dementia and neurodegeneration, the differences from control were more pronounced for late AD (VF and brain) thanearly or moderate AD (brain, VF and CSF). The findings suggest that the inclusion of metabolic, neurotrophin, stress biomarkers in AβPP-Aβ+pTau CSF-based panelscould provide more information about the status and progression of neurodegeneration, as well as aidin predicting progression from early- to late-stage AD. Furthermore, standardized multi-targeted molecular assays of neurodegeneration could help streamline postmortem diagnoses, including assessments of AD severity and pathology.

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