Chronic Traumatic Encephalopathy as the Course of Alzheimer's Disease.

This editorial investigates chronic traumatic encephalopathy (CTE) as a course of Alzheimer's disease (AD). CTE is a debilitating neurodegenerative disease that is the result of repeated mild traumatic brain injury (TBI). Many epidemiological studies show that experiencing a TBI in early or middle life is associated with an increased risk of dementia later in life. Chronic traumatic encephalopathy (CTE) and Alzheimer's disease (AD) present a series of similar neuropathological features that were investigated in this work like recombinant tau into filaments or the accumulation and aggregation of Aß protein. However, these two conditions differ from each other in brain-blood barrier damage. The purpose of this review was to evaluate information about CTE and AD from various articles, focusing especially on new therapeutic possibilities for the improvement in cognitive skills.

Chaperones-A New Class of Potential Therapeutic Targets in Alzheimer's Disease.

The review describes correlations between impaired functioning of chaperones and co-chaperones in Alzheimer's disease (AD) pathogenesis. The study aims to highlight significant lines of research in this field. Chaperones like Hsp90 or Hsp70 are critical agents in regulating cell homeostasis. Due to some conditions, like aging, their activity is damaged, resulting in ß-amyloid and tau aggregation. This leads to the development of neurocognitive impairment. Dysregulation of co-chaperones is one of the causes of this condition. Disorders in the functioning of molecules like PP5, Cdc37, CacyBP/SIPTRAP1, CHIP protein, FKBP52, or STIP1 play a key role in AD pathogenesis. PP5, Cdc37, CacyBP/SIPTRAP1, and FKBP52 are Hsp90 co-chaperones. CHIP protein is a co-chaperone that switches Hsp70/Hsp90 complexes, and STIP1 binds to Hsp70. Recognition of precise processes allows for the invention of effective treatment methods. Potential drugs may either reduce tau levels or inhibit tau accumulation and aggregation. Some substances neuroprotect from Aß toxicity. Further studies on chaperones and co-chaperones are required to understand the fundamental tenets of this topic more entirely and improve the prevention and treatment of AD.

Mitochondrial disorders leading to Alzheimer's disease-perspectives of diagnosis and treatment.

Alzheimer's disease (AD) is a neurodegenerative disorder and the most common cause of dementia globally. The pathogenesis of AD remains still unclear. The three main features of AD are extracellular deposits of amyloid beta (Aß) plaque, accumulation of abnormal formation hyper-phosphorylated tau protein, and neuronal loss. Mitochondrial impairment plays an important role in the pathogenesis of AD. There are problems with decreased activity of multiple complexes, disturbed mitochondrial fusion, and fission or formation of reactive oxygen species (ROS). Moreover, mitochondrial transport is impaired in AD. Mouse models in many research show disruptions in anterograde and retrograde transport. Both mitochondrial transportation and network impairment have a huge impact on synapse loss and, as a result, cognitive impairment. One of the very serious problems in AD is also disruption of insulin signaling which impairs mitochondrial Aß removal.Discovering precise mechanisms leading to AD enables us to find new treatment possibilities. Recent studies indicate the positive influence of metformin or antioxidants such as MitoQ, SS-31, SkQ, MitoApo, MitoTEMPO, and MitoVitE on mitochondrial functioning and hence prevent cognitive decline. Impairments in mitochondrial fission may be treated with mitochondrial division inhibitor-1 or ceramide.

Molecular cross-talk between long COVID-19 and Alzheimer's disease.

The long COVID (coronavirus disease), a multisystemic condition following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, is one of the widespread problems. Some of its symptoms affect the nervous system and resemble symptoms of Alzheimer's disease (AD)-a neurodegenerative condition caused by the accumulation of amyloid beta and hyperphosphorylation of tau proteins. Multiple studies have found dependence between these two conditions. Patients with Alzheimer's disease have a greater risk of SARS-CoV-2 infection due to increased levels of angiotensin-converting enzyme 2 (ACE2), and the infection itself promotes amyloid beta generation which enhances the risk of AD. Also, the molecular pathways are alike-misregulations in folate-mediated one-carbon metabolism, a deficit of Cq10, and disease-associated microglia. Medical imaging in both of these diseases shows a decrease in the volume of gray matter, global brain size reduction, and hypometabolism in the parahippocampal gyrus, thalamus, and cingulate cortex. In some studies, a similar approach to applied medication can be seen, including the use of amino adamantanes and phenolic compounds of rosemary. The significance of these connections and their possible application in medical practice still needs further study but there is a possibility that they will help to better understand long COVID.

Cognitive Decline in Early and Premature Menopause.

Early and premature menopause, or premature ovarian insufficiency (POI), affects 1% of women under the age of 40 years. This paper reviews the main aspects of early and premature menopause and their impact on cognitive decline. Based on the literature, cognitive complaints are more common near menopause: a phase marked by a decrease in hormone levels, especially estrogen. A premature reduction in estrogen puts women at a higher risk for cardiovascular disease, parkinsonism, depression, osteoporosis, hypertension, weight gain, midlife diabetes, as well as cognitive disorders and dementia, such as Alzheimer's disease (AD). Experimental and epidemiological studies suggest that female sex hormones have long-lasting neuroprotective and anti-aging properties. Estrogens seem to prevent cognitive disorders arising from a cholinergic deficit in women and female animals in middle age premature menopause that affects the central nervous system (CNS) directly and indirectly, both transiently and in the long term, leads to cognitive impairment or even dementia, mainly due to the decrease in estrogen levels and comorbidity with cardiovascular risk factors, autoimmune diseases, and aging. Menopausal hormone therapy from menopause to the age of 60 years may provide a "window of opportunity" to reduce the risk of mild cognitive impairment (MCI) and AD in later life. Women with earlier menopause should be taken care of by various specialists such as gynecologists, endocrinologists, neurologists, and psychiatrists in order to maintain their mental health at the highest possible level.

Correlations between Dementia and Loneliness.

This review describes associations between dementia and loneliness on the neurobiological and epidemiological levels according to the recent body of literature. The aim of this study was to highlight major lines of research in this field. Sociocognitive skills and social interactions present complex interdependencies with dementia which may be explained by two theories. According to the first one, not sufficiently engaging in social or cognitive activities results in brain atrophy. The second one claims that brain neurogenesis and synaptic density are being increased by social connections. The relationship between loneliness and dementia could be mediated by sensory loss, including hearing and visual impairment, as well as depression and psychotic symptoms. Loneliness itself might cause a depletion in sensory and cognitive stimulation which results in a decrease in neural reserve. Certain changes in the structures of the brain caused by loneliness were found in imaging examination. Loneliness appears to be a crucial risk factor for dementia in recent times due to the modern lifestyle and consequences of the outbreak of COVID-19. Additional studies are required to understand more completely the key tenets of this topic and therefore to improve the prevention and treatment of dementia.

Vocational activity for patients with multiple sclerosis.

INTRODUCTION: Multiple sclerosis (MS) usually occurs in young adults and, due to its long-lasting course and variety of symptoms, can affect their vocational activity. Our study aimed to evaluate employment status and working activity for persons with MS with regard to disease-related factors, quality of life, and depression. MATERIAL AND METHODS: 250 subjects with MS (62 men, 188 women, aged 19-71 years, mean 42.2) responded to a survey into various aspects of their employment. Relationships were sought between work-related issues and disease-related variables [MS type and duration, major symptoms, disability level on the Expanded Disability Status Scale (EDSS)], quality of life (WHOQOL- -BREF, World Health Organisation Quality of Life brief questionnaire) and depression (BDI, Beck Depression Inventory). Statistical analysis included Mann-Whitney U, Student's t, and Pearson's chi-squared tests. RESULTS: 71.2% of the patients were employed, and 49.1% perceived an impact of the disease upon their working activity (i.e. job loss, problems with finding a new one, and/or forced change of type and/or character of employment). Unemployed subjects had higher EDSS scores (4.05 vs. 2.34, p < 0.001) and longer disease durations (13.6 vs. 9.4, p < 0.001) than employed ones. They also scored higher on BDI (15.4 vs. 9.05, p < 0.001) and lower in all domains of WHOQOL-BREF (p < 0.001). CONCLUSIONS: The consequences of MS negatively influence many work-related factors. Unemployment is associated with a higher frequency of depression and a lower quality of life in MS patients.