The α-synucleinopathies are a group of neurodegenerative diseases characterized by abnormal accumulation of insoluble α-synuclein in neurons and glial cells, comprising Parkinson's disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Although varying in prevalence, symptom patterns, and severity among disorders, all α-synucleinopathies have in common autonomic nervous system dysfunctions, which reduce quality of life. Frequent symptoms among α-synucleinopathies include constipation, urinary and sexual dysfunction, and cardiovascular autonomic symptoms such as orthostatic hypotension, supine hypertension, and reduced heart rate variability. Symptoms due to autonomic dysfunction can appear before motor symptom onset, particularly in MSA and PD, hence, detection and quantitative analysis of these symptoms can enable early diagnosis and initiation of treatment, as well as identification of at-risk populations. While patients with PD, DLB, and MSA show both central and peripheral nervous system involvement of α-synuclein pathology, pure autonomic failure (PAF) is a condition characterized by generalized dysregulation of the autonomic nervous system with neuronal cytoplasmic α-synuclein inclusions in the peripheral autonomic small nerve fibers. Patients with PAF often present with orthostatic hypotension, reduced heart rate variability, anhydrosis, erectile dysfunction, and constipation, without motor or cognitive impairment. These patients also have an increased risk of developing an α-synucleinopathy with central involvement, such as PD, DLB, or MSA in later life, possibly indicating a pathophysiological disease continuum. Pathophysiological aspects, as well as developments in diagnosing and treating dysautonomic symptoms in patients with α-synucleinopathies are discussed in this review.

Objective The Face-Name Associative Memory test (FNAME) has recently received attention as a test for early diagnosis of Alzheimer’s disease. So far, however, there has been no systematic investigation of the effects of aging. Here, we aimed to assess the extent to which the FNAME performance is modulated by normal ageing. Method In a first step, we adapted the FNAME material to the Dutch population. In a second step, younger (n = 29) and older adults (n = 29) were compared on recall and recognition performance. Results Significant age effects on name recall were observed after the first exposure of new face-name pairs: younger adults remembered eight, whereas older adults remembered a mean of four out of twelve names. Although both age groups increased the number of recalled names with repeated face-name exposure, older adults did not catch up with the performance of the younger adults, and the age-effects remained stable. Despite of that, both age groups maintained their performance after a 30-min delay. Considering recognition, no age differences were demonstrated, and both age groups succeeded in the recognition of previously shown faces and names when presented along with distractors. Conclusions This study presents for the first time the results of different age groups regarding cross-modal associative memory performance on the FNAME. The recall age effects support the hypothesis of age-related differences in associative memory. To use the FNAME as an early cognitive biomarker, further subscales are suggested to increase sensitivity and specificity in the clinical context.