Several morphological changes have been described in the
choroid plexus (CP
) of Alzheimer's disease (AD) of AD patients, including flattening of epithelial cells and thickening of the irregular basement membrane, as compared to age-matched controls
[1][2][38,39]. 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][40]. Dense fibrosis of the underlying connective tissue is also present, which could be related to the increased collagen IV content, reported later
[1][2][38,39]. Biondi ring tangles, which are intracellular inclusions, were observed to be more prevalent in AD patients when compared to control individuals
[4][5][41,42]. 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][43]. 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][41,42,44]. 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][38,42,45].
The CP of AD patients and mouse AD models are also characterized by deposits of Aβ
[2][9][10][39,46,47] 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][39,48]. 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.