Background: The immune system is increasingly mentioned as a potential target for Alzheimer’s disease (AD) treatment. Objective: In the present pilot study, the effect of (neuro)inflammation on amyloidopathy was investigated in the marmoset monkey, w

SARS-CoV-2 causes acute respiratory disease, but many patients also experience neurological complications. Neuropathological changes with pronounced neuroinflammation have been described in individuals after lethal COVID-19, as well as in the CSF of hospitalized patients with neurological complications. To assess whether neuropathological changes can occur after a SARS-CoV-2 infection, leading to mild-to-moderate disease, we investigated the brains of four rhesus and four cynomolgus macaques after pulmonary disease and without overt clinical symptoms. Postmortem analysis demonstrated the infiltration of T-cells and activated microglia in the parenchyma of all infected animals, even in the absence of viral antigen or RNA. Moreover, intracellular α-synuclein aggregates were found in the brains of both macaque species. The heterogeneity of these manifestations in the brains indicates the virus’ neuropathological potential and should be considered a warning for long-term health risks, following SARS-CoV-2 infection.

Neurofeedback research in a model closely related to humans is recommended to rule out placebo effects and unspecific factors bridging the gap between nonvalidated empirical and standardized controlled research. In this article, telemetric sensorimotor rhythm (SMR; 11-14 Hz) feedback training in the marmoset monkey is applied to examine the monkey's capability to voluntary control their brain activity. Four monkeys, provided with two epidural bioelectric electrodes above the sensorimotor cortex, were trained with positive reinforcement on SMR measured by online analyses of 1.28 s electroencephalogram epochs in 30-min sessions. These monkeys learned within five sessions to increase their alpha activity. The first evidence of nonhuman primates having an operant control over the SMR is provided, an initial step for a much-needed scientific basis to neurofeedback.

Neurological compensatory mechanisms help our brain to adjust to neurodegeneration as in Parkinson’s disease. It is suggested that the compensation of the damaged striato-thalamo-cortical circuit is focused on the intact thalamo-rubro-cerebellar pathway as seen during presymptomatic Parkinson, paradoxical movement and sensorimotor rhythm (SMR). Indeed, the size of the red nucleus, connecting the cerebellum with the cerebral cortex, is larger in Parkinson’s disease patients suggesting an increased activation of this brain area. Therefore, the red nucleus was examined in MPTP-induced parkinsonian marmoset monkeys during the presymptomatic stage and after SMR activation by neurofeedback training. We found a reverse significant correlation between the early expression of parkinsonian signs and the size of the parvocellular part of the red nucleus, which is predominantly present in human and non-human primates. In quadrupedal animals it consists mainly of the magnocellular part. Furthermore, SMR activation, that mitigated parkinsonian signs, further increased the size of the red nucleus in the marmoset monkey. This plasticity of the brain helps to compensate for dysfunctional movement control and can be a promising target for compensatory treatment with neurofeedback technology, vibrotactile stimulation or DBS in order to improve the quality of life for Parkinson’s disease patients.