Abstract
We and other investigators have postulated deterioration of essential choroid plexus (CP) functions in some elderly and especially Alzheimer’s disease patients based on apparent anatomical, histological and pathological changes in CP. We have termed this putative phenomenon CP failure. By focusing on four essential energy-requiring CP functions, specifically ascorbic acid (AA) and folate transport from blood into CSF, transthyretin synthesis and secretion into CSF, and electrolyte/acid–base balance in CSF, we were able to evaluate the hypothesis of CP failure by reviewing definitive human data. In both healthy elderly and Alzheimer’s disease patients, the CP functions normally to transport AA and folates actively from blood into CSF, synthesize and secrete transthyretin into CSF, and maintain CSF acid–base balance and ion concentrations. These human CSF compositional data provide no support for the notion of CP failure in elderly humans and Alzheimer’s disease patients.
Highlights
The human choroid plexus (CP), a locus of the bloodCSF barrier (BCSFB), is an organ in the cerebral ventricles weighing approximately 2 grams [1]
Interpretation of the human data In order to evaluate CP function in the elderly and Alzheimer’s disease patients, we focus on four essential functions of the CP–ascorbic acid (AA) and folate transport from blood into Cerebrospinal fluid (CSF) via the CP, transthyretin synthesis/secretion into CSF [14], and CSF ion and pH homeostasis [2,16]
In a separate uncontrolled study of 32 Alzheimer’s patients, Bowman et al found a mean CSF/plasma ratio of 4.0 ± 0.3 (SEM)– confirming the findings summarized in Table 1. What is remarkable (Table 1) [37]
Summary
The human choroid plexus (CP), a locus of the bloodCSF barrier (BCSFB), is an organ in the cerebral ventricles weighing approximately 2 grams [1]. AA in CSF and brain of elderly and Alzheimer’s patients In a superb study using a validated, non-invasive technique with magnetic resonance spectroscopy (MRS), Emir et al showed that in the elderly (mean age 76; N = 22) the AA concentration in occipital cortex was slightly higher than in young adults (mean age 20; N = 22) [35] This MRS finding is consistent with an ample supply of AA to neurons from the CP-CSF nexus. In a separate uncontrolled study of 32 Alzheimer’s patients, Bowman et al found a mean CSF/plasma ratio of 4.0 ± 0.3 (SEM)– confirming the findings summarized in Table 1 [37] These data provide no support for abnormal AA transport function in CP of elderly or Alzheimer’s patients. The information is somewhat limited, the available evidence (CSF ion composition data from 30 Alzheimer’s patients and 50 control or normal subjects) strongly suggests that regulatory Na+, K+ and H+/HCO3transport at the BCSFB is maintained in Alzheimer’s disease [40,41,42]
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