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Background and purpose: Constipation is a common non‐motor symptom of Parkinson's disease (PD). Deposition of α‐synuclein inclusions that spread from the gut to the substantia nigra through the vagus nerve has recently been speculated to be a pre‐motor and early stage of PD. The aim of the study was to investigate whether constipation is associated with dopaminergic pathology on dopamine transporter (DAT) single‐photon emission computed tomography in early drug‐naïve patients with PD. Our hypothesis was that constipation is associated with other signs of pre‐motor PD and is independent of DAT pathology. We then investigated for associations with motor and non‐motor symptoms, and with cerebrospinal fluid biomarkers of PD pathology. Methods: Using the Parkinson's Progression Markers Initiative database, we investigated the prevalence of constipation and the association between constipation and clinical features, striatal [123I]Ioflupane uptake and non‐imaging (cerebrospinal fluid and serum) biomarkers. Constipation was evaluated using Movement Disorder Society‐Sponsored Revision of the Unified Parkinson's Disease Rating Scale (MDS‐UPDRS) Part I item 1.11. Results: One third (132/398) of de‐novo patients with PD had constipation. Higher severity of constipation correlated with older age (r = 0.728, P < 0.001), higher MDS‐UPDRS total score (r = 0.285, P < 0.001), worse postural instability (r = 0.190, P = 0.012), rapid eye movement sleep behaviour disorder (r = 0.228, P < 0.0001) and depression (r = 0.187, P = 0.024). No correlation was found with cerebrospinal fluid, serum and imaging markers of PD pathology. Conclusions: Constipation was not associated with DAT pathology but with rapid eye movement sleep behaviour disorder and depression, which are speculated to be pre‐motor symptoms of PD. This confirms the hypothesis that constipation may be a pre‐motor sign of PD due to an impairment of non‐dopaminergic pathways. [ABSTRACT FROM AUTHOR]

Background and purpose A growing body of evidence suggests that cardiovascular disease risk factors including hypertension may be linked to sporadic Alzheimer's disease (AD). It is well known that hypertension is associated with cerebrovascular disease and vascular dementia on the basis of vascular remodeling. However, the mechanisms linking hypertension and AD remain unclear. Methods We studied 197 patients with AD (86 male; mean age ± SD: 75.8 ± 7.4 years) from the Alzheimer's Disease Neuroimaging Initiative database with ( n = 97) and without ( n = 100) hypertension. We explored associations between hypertension and clinical, plasma, cerebrospinal fluid and imaging markers of AD pathology in order to elucidate the underlying mechanisms that may link AD and hypertension. Results We found that patients with AD with hypertension had worse cognitive function (Alzheimer's disease Assessment Scale-cognitive subscale, P = 0.038) and higher neuropsychiatric symptom burden (Neuropsychiatric Inventory Questionnaire, P = 0.016) compared with those without hypertension. Patients with AD with hypertension showed reduced glucose hypometabolism in the right ( P < 0.001) and left ( P = 0.007) hippocampus. No differences were found in magnetic resonance imaging volumetric measurements, [18F]florbetapir uptakes, plasma and cerebrospinal fluid between patients with AD with and without hypertension. Conclusions Although hypertension is associated with worse cognitive function, behavioural symptoms and hippocampal glucose hypometabolism, it is not associated with evidence of increased amyloid or tau pathology. Effective management of hypertension may potentially have a therapeutic role in the alleviation of symptoms in AD. [ABSTRACT FROM AUTHOR]

Levodopa-induced dyskinesias ( LIDs) and graft-induced dyskinesias ( GIDs) are serious and common complications of Parkinson's disease ( PD) management following chronic treatment with levodopa or intrastriatal transplantation with dopamine-rich foetal ventral mesencephalic tissue, respectively. Positron emission tomography ( PET) molecular imaging provides a powerful in vivo tool that has been employed over the past 20 years for the elucidation of mechanisms underlying the development of LIDs and GIDs in PD patients. PET used together with radioligands tagging molecular targets has allowed the functional investigation of several systems in the brain including the dopaminergic, serotonergic, glutamatergic, opioid, endocannabinoid, noradrenergic and cholinergic systems. In this article the role of PET imaging in unveiling pathophysiological mechanisms underlying the development of LIDs and GIDs in PD patients is reviewed. [ABSTRACT FROM AUTHOR]