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Neurovascular Dysfunction in Alzheimer Disease

Assessment of Cerebral Vasoreactivity by Ultrasound Techniques and Evaluation of Circulating Progenitor Cells and Inflammatory Markers

Cipollini, Virginia MD*; Sette, Giuliano MD, PhD*; Bossù, Paola PhD; Ciaramella, Antonio PhD; Salani, Francesca PhD; De Carolis, Antonella MD*; Troili, Fernanda MD*; Orzi, Francesco MD, PhD*; Giubilei, Franco MD, PhD*

Alzheimer Disease & Associated Disorders: July–September 2019 - Volume 33 - Issue 3 - p 212–219
doi: 10.1097/WAD.0000000000000331
Original Articles

Aims: The aims of this study were to assess vascular dysfunction in patients with Alzheimer disease (AD) by investigating cerebral vasomotor reactivity using transcranial Doppler ultrasound (TCD) and to evaluate any correlations between cerebral vasoreactivity and endothelium dysfunction. Moreover, the frequency of circulating progenitor cells (CPCs) and the blood concentration of vascular/inflammatory markers were evaluated.

Materials and Methods: We recruited 35 AD subjects and 17 age-matched, sex-matched, and education-matched healthy control subjects. Cerebral vasomotor reactivity was assessed by means of the TCD-based breath-holding index test (BHI). The level of CPCs was evaluated by means of flow cytometry from venous blood samples, while blood vascular/inflammatory markers were measured by means of enzyme-linked immunosorbent assay.

Results: Both cerebral assay blood flow velocity in the middle cerebral artery (MCAFV) and BHI values were significantly lower in AD subjects than in healthy controls (P<0.05). A positive trend was found between MCAFV and BHI values and Mini-Mental State Evaluation (MMSE) scores. Moreover, the hematopoietic progenitor cells’ count was found to be lower in patients with AD than in controls (P<0.05). Finally, a significantly higher expression of the plasma chemokine CCL-2 was observed in AD patients than in healthy controls.

Conclusions: Our results confirm that cerebral hemodynamic deterioration may be a critical marker of cognitive decline. Further studies are needed to investigate the role of circulating CPCs and chemokines as potential contributors to neurovascular dysfunction.

*NESMOS Department, Faculty of Medicine and Psychology, Sant’Andrea Hospital, Sapienza University of Rome

S. Lucia Foundation, Experimental Neuro-Psychobiology Laboratory, Clinical and Behavioral Neurology, Rome, Italy

P.B. was supported by the Italian Ministry of Health (grants RC 2016-2017-2018 and CO-2013-02356242).

The authors declare no conflicts of interest.

Reprints: Virginia Cipollini, MD, NESMOS Department, Faculty of Medicine and Psychology, Sant’Andrea Hospital, Sapienza University of Rome, Rome 00189, Italy (e-mail:

Received December 6, 2018

Accepted May 10, 2019

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