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Is Alzheimer’s Disease a Manifestation of Brain Quantum Decoherence Resulting from 

Mitochondrial and Microtubular Deterioration?

T.W. Nichols1, M.H. Berman1 and J.A. Tuszynski  2,3 

1 Quietmind Foundation, Philadelphia, PA, USA

2 Department of Physics, University of Alberta, Edmonton, AB, Canada

3 DIMEAS, Politecnico di Torino, Turin, Italy

The etiology of Alzheimer's dementia is, at best multifactorial. Before the emergence of cognitive impairment, symptoms such as thinning of the cortex, accumulation of β-amyloid, and decreased hippocampal volume are common. Hence, the accumulation of β-amyloid and hyperphosphorylated tau fibrillary tangles are two pathological hallmarks in Alzheimer's disease brains, but antibody therapy aimed to decrease β-amyloid has been a failure and, in most optimistic opinions, may delay somewhat disease progression. However, 31-38 % of subjects develop cerebral micro-hemorrhages in aducanumab therapy, an antibody to the amyloid beta plaque by Biogen. Genetics such as Apo E3/E3 have demonstrated defects in the blood-brain barrier in early-onset dementia...more

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Search for potential Alzheimer Disease therapeutics: Identification of inhibitors of amyloid oligomerization with high affinity for the zinc binding site

Elizaveta Lugovskaya, Giulia Codagnone, Ivan Sanavia, Silvia Rey, Vanessa Terranova, Marcello Miceli, Marco A. Deriu  and Jack Adam Tuszynski

The progression of Aβ peptide aggregation in the brain has been suggested to play an important role in the pathogenesis and development of Alzheimer’s disease. The present study is intended to provide insight into the interactions between the zinc binding site of beta-amyloids and the zinc ion itself. It has been amply demonstrated that the absence of zinc bonded to the beta-amyloid may slow down the progression of the Alzheimer disease, so the goal is to provide an analysis of available drugs that can be repurposed, while waiting for the development of novel therapeutics. To this end, we address the issues of how and with what strength the existing compounds bind with beta-amyloid, potentially replacing or blocking zinc and preventing it from attaching to the amyloid itself. The analysis was performed using MOE software which, starting from a filtered database, made it possible to identify the drugs that were most likely to bind to the zinc binding site on beta-amyloid.


Neurobiological circuits of anxiety and negative emotions in ASD

L.A. Cacha

ASD does not include anxiety as one of its core features, which has its own unique and additional level of complexity. The prevalence of anxiety disorder is not considered a core characteristic, yet majority of individuals with autism exhibit clinically elevated levels of anxiety or suffer from at least one anixiety disorder, including obessive-compulsive disorder. An individual who is anxious is more likely to suffer from excessive negative emotions, which are indicative of potential dysfunctions within the brain systems responsible for regulating negative emotions. Anxiety is believed to have a neurobiological component, and studies have long been conducted to determine how its arousal impacts behavioral development in typical situations. An overview of the role of the prefrontal cortex in modulation of amygdala function is presented in this paper, as well how differences in amygdala and prefrontal cortex connectivity may play a role in influencing the presentation of anxiety syndrome in the context of autism spectrum disorder.



Relationship between serum metabolic indexes and immune function in patients with insomnia and their mechanism

Zhang Sumei, Zhang Xiuhong, Wang Xiaoli, Hao Xinxin, Bai Jiangyan, and Zhao Liqiao


We conducted a study to examine how certain serum metabolic markers (reactive oxygen species (ROS), homocysteine (Hcy), and reduced glutathione (GSH)) impact the levels of IL-4 in patients with insomnia. The study involved 60 insomnia patients, including 20 with primary insomnia and 20 with somatopathy insomnia, aged 23-84 years with a mean age of 61.20 ± 12.59 years and a mean disease duration of 6.97 ± 8.45 years. There were 20 normal controls, 11 males and 9 females, aged 26-63 years, with an average age of 49.95 ± 10.52 years. We measured ROS levels using immunofluorescence, Hcy levels using enzyme-linked immunosorbent assay, and GSH levels using ELISA. The IL-4 level in serum was also detected by ELISA to assess the patient's immune function. Our analysis revealed that changes in ROS, Hcy, and GSH levels were associated with changes in IL-4 levels in serum. Therefore, early detection of serum metabolic changes in insomnia patients and proactive intervention can help reduce susceptibility to various infections and tumors.


On the transition from a sense of self to actualizing an intention

R.R. Poznanski


Action potential forms part of neural activity, but what is neural action? The generalization of specific cognitive tasks as neural cannot work, so we must individualize them, for example, intentions in action. However, the question arises: are intentions in the action part of the neural activity in the electro-ionic brain or perhaps hidden deep in the EM brain where ionization is absent? This has important implications for the experience of acting out a thought, such as subjectivity intentionality is not decipherable through neuroimaging and cannot be a viable instrument for intentions. We propose that ionization drives the transition from experience to intentions and that the experience is hidden in the unconscious and not decipherable using modern brain neuroimaging technology. The intentions are sensed through attention as feelings spontaneously and do not provide a window to subjective intentionality and its pathology in psychopathic cases.

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