Corrigendum: Psychedelics as a Treatment for Alzheimer's Disease Dementia.

[This corrects the article DOI: 10.3389/fnsyn.2020.00034.].

Psychedelics as a Treatment for Alzheimer's Disease Dementia.

Currently, there are no disease-modifying treatments for Alzheimer's disease (AD) or any other dementia subtype. The renaissance in psychedelic research in recent years, in particular studies involving psilocybin and lysergic acid diethylamide (LSD), coupled with anecdotal reports of cognitive benefits from micro-dosing, suggests that they may have a therapeutic role in a range of psychiatric and neurological conditions due to their potential to stimulate neurogenesis, provoke neuroplastic changes and reduce neuroinflammation. This inevitably makes them interesting candidates for therapeutics in dementia. This mini-review will look at the basic science and current clinical evidence for the role of psychedelics in treating dementia, especially early AD, with a particular focus on micro-dosing of the classical psychedelics LSD and psilocybin.

Subjective memory complaints after electroconvulsive therapy: systematic review.

Aims and methodFew studies have looked at subjective memory impairment from electroconvulsive therapy (ECT) after treatment completion. We aimed to systematically review all available evidence for subjective post-treatment effects. RESULTS: We included 16 studies in this review. There was considerable between-study heterogeneity in clinical population, ECT modality and assessment scales used. The most common assessment scale (eight studies) was the Squire Subjective Memory Questionnaire. The majority of studies reported an improvement in subjective memory after ECT, which correlated with improved depression scores. Subjective complaints were fewer in studies that used ultra-brief pulse ECT. Longer pulse widths were associated with more subjective complaints, as was female gender and younger age of treatment in the largest study.Clinical implicationsThere is considerable heterogeneity between studies, limiting meaningful conclusions. Ultra-brief pulse ECT appears to result in fewer subjective complaints.Declaration of interestNone.

Elevated homocysteine and N-methyl-d-aspartate-receptor antibodies as a cause of behavioural and cognitive decline in 22q11.2 deletion syndrome.

A 19-year-old male with 22q11.2 deletion syndrome presented with a 4-year history of cognitive decline and symptoms suggestive of atypical psychosis. Potential for elevated homocysteine and NMDA-receptor antibodies in the pathogenesis of his symptoms was investigated. He had elevated blood homocysteine level (18.7 µmol/l), low-normal vitamin B12 and folate levels and was positive for NMDA-receptor antibodies. Treatment with daily folinic acid (0.8 mg) and vitamin B12 (1 mg) led to dramatic improvement in his cognitive and behavioural presentation. Subsequent plasma exchange resulted in a further, significant clinical improvement. Homocysteine levels and NMDA-R antibodies should be investigated as potential causes of behavioural and cognitive symptoms in patients with 22q11.2 deletion syndrome.

Heading in football, long-term cognitive decline and dementia: evidence from screening retired professional footballers.

BACKGROUND: Heading impairs cognition in the short and medium-terms; however, little is known about the long-term consequences. This study aimed to investigate the hypothesis that chronic low-level head trauma is associated with persistent cognitive decline. METHODS: All members of Former Player Associations (FPAs) from four professional football clubs in the UK were contacted to participate in the study. Participants were required to complete a self-assessed test of cognition, the Test Your Memory questionnaire. Further information was collected from respondents in order to analyse the potential effect of a number of variables on cognition. RESULTS: 10 of 92 respondents (10.87%) screened positive for possible mild cognitive impairment (MCI) or dementia. There was no association between low-risk and high-risk playing positions (HR = 0.40, p = 0.456) or length of playing career (HR = 1.051 95% CI 0.879 to 1.257, p = 0.586) and a positive screening result. Age was a risk factor (HR = 1.137 per additional year, 95% CI 1.030 to 1.255, p < 0.05), although this was not significantly different from the population prevalence across age groups. CONCLUSIONS: These results suggest that once a player ends their playing career, their risk of harm falls in line with the population, suggesting either that changes are reversible or that heading may not be as harmful as commonly thought. Future longitudinal studies of large numbers of professional football players are needed to support the findings from this study.