Skin in the game
Persuasive new findings suggesting that detecting phosphorylated α-synuclein (ie“Lewy pathology”) in the nerves of the skin is a useful approach to the in vivo differential diagnosis of Parkinsonian disorders1 was among the topics chosen by Pascal Derkinderen (Nantes, France), who reviewed the Movement Disorders sessions.
In a study presented by Vincenzo Donadio and colleagues (University of Bologna, Italy), skin from all 26 Parkinson’s disease (PD) patients tested stained positive for α-synuclein. None of the 26 healthy controls were positive; and synuclein deposits were found in the skin of only two of 26 patients with Progressive Supranuclear Palsy or Corticobasal Syndrome.
White matter matters in progression
Progression of microstructural damage in the white matter is associated with motor and cognitive deterioration in PD, according to data from a study of 154 patients who were evaluated for cognition and had an annual MRI scan for three years.
White matter changes might provide a sensitive biomarker of disease progression, suggested Pietro Scamarcia, who presented the study on behalf of co-workers in Milan and Belgrade.
DBS electrodes cut across white matter tracts
In another white matter-related study, Guillaume Costentin and colleagues from the University Hospital, Rouen, France, evaluated 51 PD patients before and six months after deep brain stimulation of the subthalamic nucleus. Cognitive decline including reduced verbal memory was found to be associated with the frequency of white matter microlesions, especially in the superior longitudinal fasciculus.
The finding provides support for the view that cognitive side effects of DBS can arise from damage as the path of the electrodes cuts across white matter tracts involved in cognitive function.
When is AD not AD?
With the proposed move towards A/T/N classification in which 7 major Alzheimer’s disease (AD) biomarkers 3 values (+ or - A/T/N), this is not a frivolous question. One answer could be: when it is SNAP.2 Patients with Suspected Non-Alzheimer pathology (SNAP) have a pattern of neurodegeneration which looks like AD but with normal levels of amyloid-β in the brain.
Different neurodegenerative processes can underlie a similar clinical syndrome
From an overview by Philip Scheltens (Alzheimer Center Amsterdam, The Netherlands), the prevalence of SNAP in memory clinic patients seems range from 20 to 40%. In a recent series from Amsterdam, 25% of memory clinic patients were classified as SNAP (A-, T+ or T-, N-).
Mixed pathologies are common – with cerebrovascular disorders, dementia with Lewy bodies, and Frontotemporal Dementia. Underlying non-AD pathologies include primary age-related tauopathy (PART), which is found mostly in the locus coeruleus, and TDP-43 accumulation with or without hippocampal sclerosis (Limbic-Predominant TDP-43 encephalopathy, or LATE). Read more here.
In short, comorbidities are frequent; and one diagnosis can hide another, said David Wallon (University of Rouen, France) who reviewed the dementia contributions to EAN 2020 Virtual.
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