Elsevier

Neurobiology of Aging

Volume 21, Issue 1, January–February 2000, Pages 27-30
Neurobiology of Aging

Articles
Decreased high-density lipoprotein cholesterol and serum apolipoprotein AI concentrations are highly correlated with the severity of Alzheimer’s disease

https://doi.org/10.1016/S0197-4580(99)00103-7Get rights and content

Abstract

Serum apolipoprotein (apo) AI concentration was studied in 98 Alzheimer’s disease (AD) patients (77.56 ± 8.83 years) and 59 healthy, elderly controls (75.37 ± 5.27 years). ApoAI levels were significantly lower (p < 10−7) in AD patients. An apoAI cutoff value of 1.50 g/L, could distinguish between the two groups with a sensitivity of 71% and a specificity of 69%. ApoAI levels were highly correlated with mini-mental state (MMSE) scores of patients (p < 0.0001). These relationships remained significant after adjustment for multiple testing. Our findings raise the question of the potential implication of apoAI in the etiopathology of AD and bring serum apoAI concentration to the fore as an important biochemical marker.

Introduction

Apolipoprotein (apo) AI is one of the Aβ-binding proteins, the major component of senile plaques in the brain of AD patients, which includes apoE, ApoJ, transthyretin, and α-antichymotrypsin. Aβ is supposed to be under equilibrium among all factors that are thought to maintain the solubility of this peptide or to promote its deposit within the brain in some pathological conditions. ApoAI is the major component of high-density lipoprotein (HDL). Several anti-atherogenic functions have been attributed to apoAI including reverse cholesterol transport and protection against thrombosis and oxidation [13]. In cerebrospinal fluid (CSF), apoAI is also found in HDL-like particles [1], [12]. Expression of apoAI was recently reported in the brain of AD patients [5]. No significant difference in apoAI brain expression [5] or in CSF levels were found between AD patients and controls [15]. However, as shown in two studies [7], [9], plasma apoAI are reduced in AD and dementia patients. We therefore decided to re-evaluate the role of apoAI as a peripheral biochemical marker for AD and to assess its relationship with the severity of disease, as estimated by the mini-mental score (MMS) [3].

Section snippets

Subjects

The population studied included 98 late-onset AD patients (70 females and 28 males with mean age of 77.56 ± 8.85 years) as defined by the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III-R) and the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer’s Disease and Related Disorders Association of probable AD (NINCDS-ADRDA) criteria. The control group was composed of 59 supposed healthy elderly subjects (31 females and 28 males

Results

Serum apoAI levels were significantly lower (p < 10−7) in AD patients compared to controls (Table 1). The difference remained significant even when we took into account other parameters such as age, sex, and albumin as covariants. Serum levels of apoB did not differ significantly between AD patients and controls (Table 1). The levels of HDL-C-like apoAI levels, were also significantly reduced in AD patients (p < 10−7), suggesting a high association between these two parameters. The gender

Discussion

Two previous studies reported decreased levels of plasma ApoAI in AD patients [7], [9]. Our work adds to these results by studying a larger number of patients and by demonstrated for the first time that serum apoAI are highly linked to the severity of the Alzheimer’s disease, as reflected by the MMSE. ApoAI levels have been also evaluated in vascular dementia [9]. In fact, apoAI levels decreased simultaneously in both vascular dementia and Alzheimer’s diseases and cannot be used for

Acknowledgements

We thank the patients and their families for their generous cooperation, Maria Belalcazar for reviewing the paper, Dominique Aguillon for its excellent technical assistance.

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This work was partially supported by the Region Lorraine.

1

Present address: Baylor College of Medicine, Department of Cell Biology, 1 Baylor Plaza, 77030 Houston TX. E-mail address: [email protected].

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