Brain structures with bioelectric activity (BA) different from BA of the same structures in healthy peers were revealed using an original 3DLocEEG analysis of EEGs that solves so-called "reverse EEG task". These were the following structures: thalamus, pineal gland, hypothalamic area, including suprahiasmatic nuclei, and infratemporal cortex. The shift of BA focus to structures of the left hemisphere including left thalamus was recorded in patients with AIS; the shift increased both with worsening of deformation and increasing progression activity. This was not observed in healthy children (aged 7-14 years), although it is natural for older adolescents (15-17 years) and healthy adults. In other words, the interhemispheric asymmetry of brain BA in children with AIS becomes typical for the definitive brain much earlier. This phenomenon may be used for future development of a method for prediction of deformation progression patterns. A number of differences obtained in comparative analysis of EEGs, processed by 3DLocEEG method, between right-side and left-side AIS allow us to hypothesize about aetiology and pathogenesis differences of these two AIS clinical forms. Data obtained suggest that brain structures play a much more important role in aetiology and pathogenesis of AIS right-side forms compared with left-side ones. Primary subclinical dysfunctions of brain regulatory systems leading to disturbances of spinal cord and brain associated growth and subsequently to scoliosis development are supposed to play the main role in pathogenesis of right-side AIS forms (or their substantial part). Evidently, the major reason for manifesting these latent dysfunctions is an overstrain of central nervous system (CNS) adaptation-compensation mechanisms during the pubertal period.

Download full-text PDF

Source

Publication Analysis

Top Keywords

brain structures
8
analysis eegs
8
aetiology pathogenesis
8
ais
7
brain
6
structures
5
peculiarities brain
4
brain functioning
4
functioning children
4
children adolescence
4

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

Sage Bionetworks, Seattle, WA, USA.

Background: There is an urgent need for new therapeutic and diagnostic targets for Alzheimer's disease (AD). Dementia afflicts roughly 55 million individuals worldwide, and the prevalence is increasing with longer lifespans and the absence of preventive therapies. Given the demonstrated heterogeneity of Alzheimer's disease in biological and genetic components, it is critical to identify new therapeutic approaches.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Retromer Therapeutics, New York, NY, USA.

Background: Convergent evidence indicates that deficits in the endosomal recycling pathway underlies pathogenesis of Alzheimer's disease (AD). SORL1 encodes the retromer-associated receptor SORLA that plays an essential role in recycling of AD-associated cargos such as the amyloid precursor protein and the glutamatergic AMPA receptor. Importantly, loss of function pathogenic SORL1 variants are associated with AD.

View Article and Find Full Text PDF

Background: Alzheimer's disease (AD) is the most prevalent cause of dementia accounting for an estimated 60% to 80% of cases. Despite advances in the research field, developing truly effective therapies for AD symptoms remains a major challenge. Sweet almond contain nutrients that have the potential of combating age-related brain dysfunction, by improving learning, memory and neurocognitive performance.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

ADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea, Republic of (South).

Background: The spatiotemporal pattern of the spread of pathologically modified tau through brain regions in Alzheimer's disease (AD) can be explained by prion-like cell-to-cell seeding and propagation of misfolded tau aggregates. Hence, to develop targeted therapeutic antibodies, it is important to identify the seeding- and propagation-competent tau species. The hexapeptide VQIINK of tau is a critical region for tau aggregation, and K280 is acetylated in various tauopathies including AD.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Biosplice Therapeutics, Inc., San Diego, CA, USA.

Background: DYRK1A overexpression, common in neurodegenerative diseases like Alzheimer's (AD), contributes to neurofibrillary tangles via Tau protein hyperphosphorylation and amyloid plaque formation, key AD hallmarks. Therefore, DYRK1A has been regarded as a novel target for neurodegenerative diseases. However, developing DYRK1A selective inhibitors has been a difficult challenge due to the highly conserved ATP-binding site of protein kinases, particularly among the CMGC family.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!