According to the amyloid theory, the appearance of amyloid-β (Aβ) deposits represents a pivotal event in late onset Alzheimer's disease (LOAD). Physiologically, Aβ42 monomers are cleaned by capillary resorption, enzymatic catabolism, and cerebrospinal fluid (CSF) transport. Factors that promote the oligomerization of Aβ42 must be specified. In vitro, these monomers spontaneously form neurotoxic oligomers whose rate increases with time suggesting that the stasis of CSF favors the oligomerization. In animals, experimental hydrocephalus generates CSF stasis followed by the appearance of amyloid deposits. In normal pressure hydrocephalus, amyloid deposits are common, especially in elderly patients, and the turnover decline has the same order of magnitude as in AD. In this disease, the effects of CSF stasis are potentiated by the decline in the ability of CSF to inhibit the formation of oligomers. CSF originates from choroid plexus (CP). In LOAD, the functions of secretion, synthesis, and transport of CP are impaired and this is related to morphological modifications. These impairments favor the decrease of CSF turnover, the diminished levels of transthyretin, a sequestering protein synthesized by CP, and the oligomerization of Aβ42. They are potentiated by a reduced enzymatic catabolism and a decreased capillary reabsorption of Aβ42, both alterations being related to age.

Anticholinergic burden appears as a risk factor for both delirium symptoms and mortality. Prevention of delirium symptoms requires its reduction.

The decrease in CP permeability is in line with the age-related changes in CSF secretion observed in animals. The MTT increase indicates significant structural changes corroborated by microscopy studies in animals or humans. Overall, DSC MR-perfusion enables an in vivo evaluation of the hemodynamic state of CP. Clinical applications such as neurodegenerative diseases could be considered thanks to specific functional studies of CP.

Although AD and NPH both involve CSF disorders, the two diseases do not have the same impact on the internal capsules. The magnitude of the ADC is related to the aqueductal CSF stroke volume in AD, whereas FA is related to ventricular volume in NPH.

Purpose. This work suggests a fast estimation method of the lateral ventricles volume from a 2D image and then determines if this volume is correlated with the cerebrospinal fluid flow at the aqueductal and cerebral levels in neurodegenerative diseases. Materials and Methods. FForty-five elderly patients suffering from Alzheimer's disease (19), normal pressure hydrocephalus (13), and vascular dementia (13) were involved and underwent anatomical and phase contrast MRI scans. Lateral ventricles and stroke volumes were assessed on anatomical and phase contrast scans, respectively. A common reference plane was used to calculate the lateral ventricles' area on 2D images. Results. The largest volumes were observed in hydrocephalus patients. The linear regression between volumes and areas was computed, and a strong positive correlation was detected (R 2 = 0.9). A derived equation was determined to represent the volumes for any given area. On the other hand, no significant correlations were detected between ventricles and stroke volumes (R 2 ≤ 0.15). Conclusion. Lateral ventricles volumes are significantly proportional to the 2D reference section area and could be used for patients' follow-up even if 3D images are unavailable. The cerebrospinal fluid fluctuations in brain disorders may depend on many physiological parameters other than the ventricular morphology.

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In the original paper, the authors' given and last names were inverted. Here we provide the right authors' information as shown above.