Connecting Mind-Body Therapy-Mediated Effects to Pathological Features of Alzheimer's Disease.

Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disorder that represents a major and increasing global health challenge. In most cases, the first clinical symptoms of AD are preceded by neuropathological changes in the brain that develop years to decades before their onset. Therefore, research in the last years has focused on this preclinical stage of AD trying to discover intervention strategies that might, if implemented effectively, delay or prevent disease progression.

Re-thinking the Etiological Framework of Neurodegeneration.

Neurodegenerative diseases are among the leading causes of disability and death worldwide. The disease-related socioeconomic burden is expected to increase with the steadily increasing life expectancy. In spite of decades of clinical and basic research, most strategies designed to manage degenerative brain diseases are palliative.

The Color of Noise and Weak Stationarity at the NREM to REM Sleep Transition in Mild Cognitive Impaired Subjects.

In Older Adults (OAs), Electroencephalogram (EEG) slowing in frontal lobes and a diminished muscle atonia during Rapid Eye Movement sleep (REM) have each been effective tracers of Mild Cognitive Impairment (MCI), but this relationship remains to be explored by non-linear analysis. Likewise, data provided by EEG, EMG (Electromyogram) and EOG (Electrooculogram)-the three required sleep indicators-during the transition from REM to Non-REM (NREM) sleep have not been related jointly to MCI. Therefore, the main aim of the study was to explore, with results for Detrended Fluctuation Analysis (DFA) and multichannel DFA (mDFA), the Color of Noise (CN) at the NREM to REM transition in OAs with MCI vs.

Synergistic Effect on Neurodegeneration by N-Truncated Aβ and Pyroglutamate Aβ in a Mouse Model of Alzheimer's Disease.

The N-terminally truncated pyroglutamate Aβ (Aβ) and Aβ peptides are known to be highly abundant in the brain of Alzheimer's disease (AD) patients. Both peptides show enhanced aggregation and neurotoxicity in comparison to full-length Aβ, suggesting that these amyloid peptides may play an important role in the pathogenesis of AD. The aim of the present work was to study the direct effect of the combination of Aβ and Aβ on ongoing AD-related neuron loss, pathology, and neurological deficits in transgenic mice.

Abeta targets of the biosimilar antibodies of Bapineuzumab, Crenezumab, Solanezumab in comparison to an antibody against N‑truncated Abeta in sporadic Alzheimer disease cases and mouse models.

Solanezumab and Crenezumab are two humanized antibodies targeting Amyloid-β (Aβ) which are currently tested in multiple clinical trials for the prevention of Alzheimer's disease. However, there is a scientific discussion ongoing about the target engagement of these antibodies. Here, we report the immunohistochemical staining profiles of biosimilar antibodies of Solanezumab, Crenezumab and Bapineuzumab in human formalin-fixed, paraffin-embedded tissue and human fresh frozen tissue.