Several morphological changes have been described in the choroid plexus (CP) of Alzheimer's disease (AD) patients, including flattening of epithelial cells and thickening of the irregular basement membrane, as compared to age-matched controls
[1][2]. Aβ may also induce morphological changes in the CP cells, such as nucleus and cell volume shrinkage, as shown by CPECs from Aβ-injected mice
[3]. Dense fibrosis of the underlying connective tissue is also present, which could be related to the increased collagen IV content, reported later
[1][2]. Biondi ring tangles, which are intracellular inclusions, were observed to be more prevalent in AD patients when compared to control individuals
[4][5]. Despite the discovery of Biondi body-like inclusions in an elderly chimpanzee, these inclusions were only ever detected in aged human CP, making their study difficult
[6]. Histological analysis revealed several proteins constituting these aggregates, including tau protein, fibronectin, ubiquitin, and P component, as well as the presence of lipid droplets. The occurrence of these structures in the cytoplasm can cause mechanical damage to the plasma membrane
[4][5][7]. Lipofuscin granules, which arise from highly oxidized cross-linked macromolecules and affect vesicle trafficking and cellular physiology, are also found in the cytoplasm of choroid plexus epithelial cells (CPECs) from aged and AD mice
[1][5][8].
The CP of AD patients and mouse AD models are also characterized by deposits of Aβ
[2][9][10] that may disrupt several CP functions. However, the alterations described are not exclusive of the AD brain and have been reported in aged mice
[2][11]. Nevertheless, Aβ seems to play a crucial role in the degeneration of the biochemical pathways of the brain, including in the CP, as detailed in the sections below.