| Literature DB >> 20847429 |
Bernhard Rosengarten1, Veren Dannhardt, Ole Burr, Matthias Pöhler, Susanne Rosengarten, Matthias Oechsner, Iris Reuter.
Abstract
Alzheimer's disease (AD) and Parkinson's disease (PD) lead to a cholinergic deficit in the brain which is not only related to dementia, but may also lead to a disturbed neurovascular coupling. We investigated the effect of cholinergic decline on neurovascular coupling in PD patients. Patients with idiopathic PD were divided in groups without (n=59; 65 ± 9 y) or with moderate dementia as specified by Mini-Mental State Examination. The demented patients were assigned to groups with (n=55; 73 ± 6 y) or without (n=61; 72 ± 8 y) acetylcholinesterase inhibitor treatment. Neurovascular coupling was assessed by a simultaneous electroencephalography-Doppler technique applying a contrast-based visual stimulation task. Visually evoked potential amplitudes (N75-P100) and parameters of the hemodynamic response in the posterior cerebral artery were obtained using a control system approach (resting flow velocity, gain, attenuation, rate time, and natural frequency). Data were compared to a healthy control group of a similar age range (n=20; 63 ± 8 yr). Compared to controls, patient groups presented no differences in evoked potential amplitudes or neurovascular coupling parameters. The reported 30% decline in acetylcholinesterase activity in PD patients did not lead to measurable changes in neurovascular coupling. In AD patients additional factors might explain the uncoupling and higher cerebrovascular risk detected in clinical studies.Entities:
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Year: 2010 PMID: 20847429 DOI: 10.3233/JAD-2010-101140
Source DB: PubMed Journal: J Alzheimers Dis ISSN: 1387-2877 Impact factor: 4.472