Old age increases the risk of Alzheimer’s disease (AD), the most common neurodegenerative disease, a devastating disorder of the human mind and the leading cause of dementia. Worldwide, 50 million people have the disease, and it is estimated that there will be 150 million by 2050. Today, healthcare for AD patients consumes 1% of the global economy. According to the amyloid cascade hypothesis, AD begins in the brain by accumulating and aggregating Aβ peptides and forming β-amyloid fibrils (Aβ42). However, in clinical trials, reducing Aβ peptide production and amyloid formation in the brain did not slow cognitive decline or improve daily life in AD patients. Prevention studies in cognitively unimpaired people at high risk or genetically destined to develop AD also have not slowed cognitive decline. These observations argue against the amyloid hypothesis of AD etiology, its development, and disease mechanisms. Here, we look at other avenues in the research of AD, such as the presenilin hypothesis, synaptic glutamate signaling, and the role of astrocytes and the glutamate transporter EAAT2 in the development of AD.

Beginning with the various strategies of the SARS-CoV-2 virus to invade our bodies and manifest infection, and ending with the recent long COVID, we are witnessing the evolving course of the disease in addition to the pandemic. Given the partially controlled course of the COVID-19 pandemic, the greatest challenge currently lies in managing the short- and long-term complications of COVID-19. We have assembled current knowledge of the broad spectrum of cardiovascular, pulmonary, and neuropsychiatric sequelae following SARS-CoV-2 infection to understand how these clinical manifestations collectively lead to a severe form of the disease. The ultimate goal would be to better understand these complications and find ways to prevent clinical deterioration.

Women have an over 50% greater risk of dementia than men, which is a main topic of much research. This review aims to investigate the impact of a woman’s reproductive history on dementia risk. The consequences of stillbirth are long-term health and psychosocial problems for women. Because of the awareness of an endangered pregnancy, many parents experience deep anxiety and stress in subsequent pregnancies. There are contradictory conclusions from research about abortion and the risk of dementia correlation. When it comes to the late age of first birth, which is said to be above 35 years old, it was observed that older mothers have a decreased risk of dementia compared to those who gave birth in their 20s; however, being a child of the older mother is connected with a higher risk of developing dementia. Using hormonal contraception can result in decreased risk of dementia as estrogen stimulates microglia-related Aβ removal and reduces tau hyperphosphorylation. The influence of postmenopausal hormonal therapy and the duration of the reproductive period on developing dementia remains unclear. Although female disorders like endometriosis and polycystic ovary syndrome are reported to increase the risk of dementia, the research on this topic is very limited, especially when it comes to endometriosis, and needs further investigation. Interestingly, there is no conclusion on whether hypertensive disorders of pregnancy increase the risk of dementia, but most articles seem to confirm this theory.

Parkinson’s disease (PD) is a neurodegenerative disorder involving decreased dopamine release and atrophy of dopaminergic neurons of the substantia nigra. Frailty syndrome (FS) is common in older adults, which, in combination with PD symptoms, can substantially affect the quality of life (QOL). This study aimed to assess the prevalence of FS among PD patients and to identify variables affecting their QOL with particular attention to FS. The study included 296 patients (n = 173 women) with a mean age of 70.3 ± 5.7 years suffering from PD for an average of 8.2 ± 5.6 years. Patients were classified as at least stage II according to the Hoehn and Yahr scale. The following standardized questionnaires were used in the study: Schwab and England Activities of Daily Living (SE-ADL), Parkinson’s Disease Questionnaire (PDQ-39), Beck Depression Inventory (BDI), Unified Parkinson’s Disease Rating Scale (UPDRS), and Tilburg Frailty Indicator (TFI). FS was found in 96% (n = 283) of the PD patients studied. No depression occurred in 30% (n = 89) of subjects, moderate depression in 48% (n = 141) of subjects, and severe depression in 22% (n = 66) of subjects. The mean score of the PDQ-39 questionnaire in PD subjects with FS was 41.6 pts (min–max: 5.2–81.5 pts; SD = 17.4 pts), which was statistically significantly higher than in subjects without FS (p < 0.05). FS has been shown to be present in most of the subjects with PD. FS occurs more frequently with a longer PD period, which is associated with reduced physical capacity and QOL. Physical activity improves QOL and reduces disease progression. FS, similar to PD, is a common cause of disability in older adults and their dependency. Predictors such as depression, advanced stage of the disease, higher education, and low professional and economic status significantly affect the QOL level of PD patients. However, the results obtained among the Polish population of PD patients do not confirm the impact of FS on the QOL, so there is a need to conduct further research on this subject.

Alzheimer’s disease (AD) is the most common cause of dementia worldwide. Pathological deposits of neurotoxin proteins within the brain, such as amyloid-β and hyperphosphorylated tau tangles, are prominent features in AD. The prion protein (PrP) is involved in neurodegeneration via its conversion from the normal cellular form (PrPC) to the infection prion protein scrapie (PrPSc) form. Some studies indicated that post-translationally modified PrPC isoforms play a fundamental role in AD pathological progression. Several studies have shown that the interaction of Aβ oligomers (Aβos) with the N-terminal residues of the PrPC protein region appears critical for neuronal toxicity. PrPC-Aβ binding always occurs in AD brains and is never detected in non-demented controls, and the binding of Aβ aggregates to PrPC is restricted to the N-terminus of PrPC. In this study, we aimed to gather all of the recent information about the connections between PrPC and AD, with potential clinical implications.