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Patients with Parkinson's disease (PD) exhibit a domain-general visuospatial dysfunction; however, no previous study has examined changes over time in forward and backward spatial recall in PD against controls. To evaluate changes in short-term (STM) and working memory (WM) dysfunction in PD, the current study assessed performance on a computer-modified version of the Corsi Block-Tapping Test (forward and backward recall) at two-time points 1 year apart, while simultaneously exploring associations with potentially relevant demographic and clinical variables. We enrolled 38 patients with PD and 38 controls matched for age, sex, and Montreal Cognitive Assessment (MoCA) total scores. Linear mixed-effects models analyzed the primary measured variables (forward and backward scores). At baseline, the dysfunction effect sizes were as follows: forward recall (−0.45, 95% CI [−0.90, 0.01]) and backward recall (−0.26, 95% CI [−0.71, 0.19]). At follow-up, patients exhibited substantially greater difficulties in backward recall (−0.65, 95% CI [−1.18, −0.13]) compared to the baseline assessment, whereas the forward dysfunction effect size remained almost the same (−0.43, 95% CI [−0.94, 0.09]). Age (p =.005, f = 0.35) and total scores on MoCA (p =.017, f = 0.18), irrespective of group and recall condition, were significant predictors of spatial block scores. The pattern of dysfunction effect sizes indicates that, in contrast to forward recall, backward recall dysfunction in PD worsened 1-year after the baseline assessment, presumably reflecting the progression of PD-related visuospatial WM dysfunction. [ABSTRACT FROM AUTHOR]

Aotearoa New Zealand's population is ageing. Increasing life expectancy is accompanied by increases in prevalence of Alzheimer's Disease (AD) and ageing-related disorders. The multicentre Dementia Prevention Research Clinic longitudinal study aims to improve understanding of AD and dementia in Aotearoa, in order to develop interventions that delay or prevent progression to dementia. Comprising research clinics in Auckland, Christchurch and Dunedin, this multi-disciplinary study involves community participants who undergo biennial investigations informed by international protocols and best practice: clinical, neuropsychological, neuroimaging, lifestyle evaluations, APOE genotyping, blood collection and processing. A key research objective is to identify a 'biomarker signature' that predicts progression from mild cognitive impairment to AD. Candidate biomarkers include: blood proteins and microRNAs, genetic, neuroimaging and neuropsychological markers, health, cultural, lifestyle, sensory and psychosocial factors. We are examining a range of mechanisms underlying the progression of AD pathology (e.g. faulty blood–brain barrier, excess parenchymal iron, vascular dysregulation). This paper will outline key aspects of the Dementia Prevention Research Clinic's research, provide an overview of data collection, and a summary of 266 participants recruited to date. The national outreach of the clinics is a strength; the heart of the Dementia Prevention Research Clinics are its people. [ABSTRACT FROM AUTHOR]

Background: Advances in ultra‐sensitive immunoassay methods, like Single molecule array (Simoa) technology, show that Alzheimer's disease (AD) neuropathology can be detected in blood at the earliest stages of AD. This study compared cross‐sectional biomarker profiles for participants from the New Zealand‐Dementia Prevention Research Clinics (NZ‐DPRCs) who spanned the continuum from healthy older adults to a clinical diagnosis of AD. Method: Blood plasma samples were obtained from 253 NZ‐DPRC participants (aged 55 to 87) from their baseline assessment. Participants were classified as cognitively normal adults (CN, n = 34), subjective cognitive decline (SCD, n = 64), non‐amnestic mild cognitive impairment (single and multi‐domain, non‐aMCI, n = 23), amnestic MCI (single and multi‐domain, aMCI, n = 105), and AD (n = 27). Six plasma biomarkers were selected for quantification by the HD‐X Simoa analyser (Quanterix, Billerica, MA; University of Gothenburg, Sweden): AD biomarkers amyloid‐beta peptides (Aß1‐40; Aß1‐42) and phosphorylated tau species (p‐tau181; p‐tau231); neurofilament light (NfL), for general neuronal damage; and glial fibrillary acidic protein (GFAP), for astrocyte activation. Clinical, imaging and genetic demographic data were assessed in relation to the plasma biomarkers. Result: Plasma biomarkers across the five groups (figure 1) were assessed by linear regression adjusted for age and sex. P‐tau181, p‐tau231, GFAP and NfL were natural log‐transformed to approximate normality and improve homogeneity of variance. Biomarkers p‐tau181, p‐tau231, GFAP, NfL, Aß1‐42/Aß1‐40 ratio and Aß1‐42, all showed group effects (P < 0.05; Aß1‐40, p<0.08). Tukey's HSD post‐hoc test for pairwise group comparisons showed significant differences in GFAP for AD vs CN, SCD, non‐aMCI as well as SCD vs MCI (P < 0.05); p‐tau181 for AD vs CN and SCD (P < 0.05); p‐tau231 for AD vs non‐aMCI (P < 0.05); Aß1‐42 for aMCI vs CN and SCD (P < 0.05); Aß1‐42/Aß1‐40 ratio for SCD vs aMCI (P < 0.05). ROC analysis will be reported for the diagnostic accuracy of these blood analytes. Conclusion: Simoa‐quantitated blood biomarkers in the NZ‐DPRC cohort differentiates clinical groups spanning the AD continuum cross‐sectionally. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented discussing the association of a spontaneous internal carotid artery dissection (CAD) with cerebral aneurysms and thin glomerular basement membrane nephropathy.

Introduction: Early intervention in Alzheimer's disease (AD) requires the development of an easily administered test that is able to identify those at risk. Focusing on microRNA robustly detected in plasma and standardizing the analysis strategy, we sought to identify disease-stage specific biomarkers., Methods: Using TaqMan microfluidics arrays and a statistical consensus approach, we assessed plasma levels of 185 neurodegeneration-related microRNA, in cohorts of cognitively normal amyloid β-positive (CN-Aβ+), mild cognitive impairment (MCI), and Alzheimer's disease (AD) participants, relative to their respective controls., Results: Distinct disease stage microRNA biomarkers were identified, shown to predict membership of the groups (area under the curve [AUC] >0.8) and were altered dynamically with AD progression in a longitudinal study. Bioinformatics demonstrated that these microRNA target known AD-related pathways, such as the Phosphoinositide 3-kinase (PI3K-Akt) signalling pathway. Furthermore, a significant correlation was found between miR-27a-3p, miR-27b-3p, and miR-324-5p and amyloid beta load., Discussion: Our results show that microRNA signatures alter throughout the progression of AD, reflect the underlying disease pathology, and may prove to be useful diagnostic markers., Competing Interests: Helen Tsui: nothing to disclose Chris J. Fowler: nothing to disclose Colin L. Masters: nothing to disclose Ralph N. Martins: nothing to disclose Nicholas J. Cutfield: Attended conferences and workshops for which costs were subsidized, but received no direct payments. Allergan‐sponsored Movement disorders injectors workshop, Hamilton NZ (2019); Biogen and Roche‐sponsored Multiple Sclerosis meetings (2018, 2019, 2020), (2019); Biogen‐sponsored Multiple Sclerosis ATLAS meeting, Sydney Australia; Sanofi American Academy of Neurology meeting, California, USA., (© 2021 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer's Association.)