Mini-Review on Lipofuscin and Aging: Focusing on The Molecular Interface, The Biological Recycling Mechanism, Oxidative Stress, and The Gut-Brain Axis Functionality.

Intra-lysosomal accumulation of the autofluorescent "residue" known as lipofuscin, which is found within postmitotic cells, remains controversial. Although it was considered a harmless hallmark of aging, its presence is detrimental as it continually accumulates. The latest evidence highlighted that lipofuscin strongly correlates with the excessive production of reactive oxygen species; however, despite this, lipofuscin cannot be removed by the biological recycling mechanisms. The antagonistic effects exerted at the DNA level culminate in a dysregulation of the cell cycle, by inducing a loss of the entire internal environment and abnormal gene(s) expression. Additionally, it appears that a crucial role in the production of reactive oxygen species can be attributed to gut microbiota, due to their ability to shape our behavior and neurodevelopment through their maintenance of the central nervous system.

Treatment of Epilepsy Associated with Common Chromosomal Developmental Diseases.

Chromosomal diseases are heterogeneous conditions with complex phenotypes, which include also epileptic seizures. Each chromosomal syndrome has a range of specific characteristics regarding the type of seizures, EEG findings and specific response to antiepileptic drugs, significant in the context of the respective genetic etiology. Therefore, it is very important to know these particularities, in order to avoid an exacerbation of seizures or some side effects. In this paper we will present a review of the epileptic seizures and antiepileptic treatment in some of the most common chromosomal syndromes.

Neurofibromatosis type 1 associated with moyamoya syndrome. Case report and review of the literature.

Neurofibromatosis type 1 (NF1) is a genetic disorder with a very heterogeneous clinical picture, affecting central nervous system, skin and bone system. Cerebrovascular lesions, such as moyamoya syndrome, are rarely seen in NF1. Approximately 250 children with NF1 and moyamoya syndrome have been reported. The clinical picture includes hemiparesis, hemianopsia, paresthesia, seizures, speech disorders, and intellectual disability. In this paper, we report on a 6-year-old girl with NF1 and moyamoya syndrome, with a brief review of the existing literature.

Longevity health sciences and mental health as future medicine.

Longevity health sciences and mental health are fields of public health and of preventive and integrative medicine. The antagonism between health construction and human pathology is substantiated by two opposite fundamental pathways: the health-longevity tetrad versus the aging-disease cascade. It is necessary that the current paradigm of contemporary medicine be replaced by the advanced paradigm of future medicine. A societal cost-benefit rate is decisive for health-longevity promotion. This is why the WHO public health strategy keeps forwarding the societal medical target into the global health-longevity field.

Brain lipopigment accumulation in normal and pathological aging.

A principal marker of brain vulnerability, stress, aging, and related pathology is represented by lipopigments (LPs)--lipofuscin, and ceroid. During ontogenesis, neuronal LP accumulations are significantly correlated with important changes in nerve cell morphology and biochemistry. In the aged neurons, LPs are present in all cellular compartments. Moreover, neuronal LP accumulations coexist with glial LP storage, especially in microglia. Owing to their transporting properties, and the migration capacity of microglia, glial cells deposit LP clusters in pericapillary areas. Thus, LP conglomerates appear in the whole nervous tissue, creating specific patterns of LP architectonics. Direct interrelations, critical LP concentrations, which generate cascades of negative subcellular events, and indirect impairment correlations determine characteristic neuropathologic aging profiles. These specific and associated negative neuropathologic consequences of LP accumulation have multiple and detrimental impacts on neuron and glia homeostasis, ranging from neuronal function to central nervous system physiology.

Processing, lysis, and elimination of brain lipopigments in rejuvenation therapies.

Cerebral lipopigments (LPs)--lipofuscin and ceroid--represent a significant marker in postmitotic normal and pathologic aging, connected with causal and associated neuropathologic damage. Therefore, LP processing, lysis, and elimination may be the main targets in anti-aging and rejuvenation therapies. The regenerative neuroactive factors improve neuron supply with specific nutrients from plasma. They enhance the antioxidative defense, have anti-LP-poietic actions, stimulate brain anabolism, support energetic metabolism, and elevate the reduced lysosomal enzymes. In the second stage, by cytoplasm rehydration, they initiate the breaking up of the neuronal aggregated LP conglomerates, by consecutive disintegration. Then, possibly by the localized exo-endocytosis process between neurons and adjacent glia (especially microglia), intercellular LP transfer can be realized. So, therapeutically activated glia turn into brain garbage collectors and transporters. Therapeutic processing of glial LPs increases in the capillary neighborhood. Highly processed LPs, by glio-endothelial transfer, reach capillary walls before being eliminated. Consequently, neuroactive therapies having these synergistic rejuvenative actions represent new prospects in deceleration of normal and pathological cerebral aging.