At present, the treatment of Alzheimer’s disease involves only symptomatic medications which have continually demonstrated little efficacy, primarily due to the presence of biological barriers. Despite efforts, researchers have yet to discover a therapeutic treatment that delays neurodegenerative progression or restores associated Alzheimer neuropathological processes. For centuries, Hericium erinaceus (HE) has been used predominantly in Asian countries for its culinary and medicinal purposes, however, the use of this mushroom has not yet been utilised in western pharmacology. This review systematically investigates evidence pertaining to the use of HE as a potential future therapeutic treatment for the prevention and delayed progression of Alzheimer’s disease, by highlighting any fundamental neurotrophic and neuroprotective properties. In total, 3 human clinical trials and 13 animal-model studies were included for review. The use of HE demonstrated positive significant differences in results obtained from behavioural, histological, and biochemical assessments from both human clinical trials and animal model studies accentuating its utility for the improvement of cognitive function. In addition, erinacine A enriched HE appears to demonstrate the highest bioactive potency of all HE extracted compounds providing the greatest effects, while also evidencing transportability ease across biological barriers. In conclusion, evidence suggests that an intake of HE may be an appropriate and relevant future therapeutic treatment for the prevention and delayed progression of Alzheimer’s disease, however, continued research is necessary to provide increased significant evidence of this relationship, most likely through the increased quantity of human clinical trials.

The introduction of portable MRI (pMRI) has the potential to directly impact dementia research and ultimately clinical care. In this paper, we explore two ethical challenges facing the introduction of pMRI in dementia research. The first is the need to ensure that pMRI enhances rather than undermines efforts aimed at improving ethnoracial representation in dementia research. The second is the need to implement pMRI in dementia research in a dementia-friendly way that attends to the social context and lived experience of people with dementia.

Introduction: Motor impairment remains underexplored in Alzheimer’s disease. We previously described the functional impairment of gait and exploratory activity of male 3xTg-AD mice at different stages of Alzheimer’s disease progression. We describe movement limitations and muscle weakness as indicators of severity.

Methods: In the present report, a cross-sectional study was carried out that analyzed the muscular structure of the quadriceps and triceps surae muscles of transgenic (3xTg-AD) and non-transgenic males in the early (6 months), intermediate (12 months), and advanced (16 months) stages of Alzheimer’s disease. Longitudinal sections of the quadriceps and triceps surae stained with hematoxylin and eosin (H&E) were evaluated. Using conventional histological techniques, they were then rinsed with PBS, pH 7.4. For the F-actine immunohistochemistry, the sections were blocked by incubating them in IgG-free 2% bovine serum albumin (BSA, Sigma) for 60 min. Then specimens were incubated for 10 minutes with 0.2% Triton X-100 in PBS at room temperature. The slides were incubated overnight at 4 °C with F-actin (Santa Cruz Biotechnology Inc., CA, USA). Slides were counterstained with VectaShield using 4, 60-diamino-2-phenylindole dihydrochloride (DAPI) (Vector Labs., CA, USA) for nuclei staining and visualized in the blue channel.

Results: Lower fluorescence labeling was detected in 3xTg-AD mice at all ages, with a greater decline at older ages. Signs of sarcopenia are also present in an advanced stage of AD, with differences in fiber distribution, the number of cell nuclei, and the presence of adipose tissue.

Conclusions: The previously reported gait alterations in Alzheimer’s disease could be the result of structural deficiencies due to sarcopenia and poor muscle contraction, which leads to the limitations of movement in locomotion reported in 3xTg-AD mice.

Objective: Patients with cognitive disorders such as Alzheimer’s disease (AD) and mild cognitive impairment (MCI) frequently exhibit depressive symptoms. Depressive symptoms can be evaluated with various measures and questionnaires. Geriatric Depression Scale (GDS) is a scale that can be used to measure symptoms in geriatric age. Many questionnaires usually sum up symptom scales. However, core symptoms of depression in these patients and connections between these symptoms have not been fully explored yet. Thus, the objectives of this study were: 1) to determine core symptoms of two cognitive disorders, Alzheimer’s disease and mild cognitive impairment; and 2) to investigate the network structure of depressive symptomatology in individuals with cognitive impairment in comparison with those with Alzheimer’s disease.

Methods: This study encompassed 5,354 patients with cognitive impairments such as Alzheimer’s disease [n = 1,889] and mild cognitive impairment [n = 3,464]. The Geriatric Depression Scale, a self-administered questionnaire, was employed to assess depressive symptomatology. Using exploratory graph analysis (EGA), a network analysis was conducted and the network structure was evaluated through regularized partial correlation models. To determine the centrality of depressive symptoms within each cohort, network parameters such as strength, betweenness, and closeness were examined. Additionally, to explore differences in the network structure between Alzheimer’s disease and mild cognitive impairment groups, a network comparison test was performed.

Results: In the analysis of centrality indices, “worthlessness’’ was identified as the most central symptom in the Geriatric Depression Scale among patients with Alzheimer’s disease, whereas “emptiness’’ was found to be the most central symptom in patients with mild cognitive impairment. Despite these differences in central symptoms, the comparative analysis showed no statistical difference in the overall network structure between Alzheimer’s disease and mild cognitive impairment groups.

Conclusion: Findings of this study could contribute to a better understanding of the manifestation of depressive symptoms in patients with cognitive impairment. These results are expected to aid in identifying and prioritizing core symptoms in these patients. Further research should be conducted to explore potential interventions tailored to these core symptoms in patients with Alzheimer’s disease and mild cognitive impairment. Finding out core symptoms in those groups might have clinical importance in that appropriate treatment for neuropsychiatric symptoms in patients with cognitive impairment could help preclude progression tofurtherimpairment.

Introduction: People with young-onset Alzheimer’s disease (YOAD) are diagnosed when the neurocognitive process begins before the age of 65 and often present with more global impairments and a more rapid course of the disease. In contrast, in late-onset Alzheimer’s disease (LOAD), the loss of short-term memory is most pronounced. Therefore, the age of onset may affect global functioning in different ways.

Objectives: This study examines the relationship between Social Cognition, global cognition, and other clinical variables in young and late-onset people with Alzheimer’s disease and their caregivers.

Methods: Using a cross-sectional design, we included 48 people with YOAD and 118 with LOAD and their carers. We assessed social cognition, global cognition, quality of life, dementia severity, mood, functionality, neuropsychiatric symptoms, and caregiver burden.

Results: Our results showed that the YOAD group had more global cognitive impairment, lower MMSE scores (P = 0.018, d = 0.41), higher Adas cog (P = 0.002, d = 0.06), poorer quality of life (QoL- AD) (P = 0.036, d = 0.36), and more neuropsychiatric symptoms (NPI) (P = 0.044, d = 0.35). However, social cognition showed a stable pattern of impairments in YOAD that did not follow the global deficits. The multifactorial regression analyses further showed that in both groups functionality was significantly related to Social Cognition, YOAD (P = 0.035), and LOAD (P = 0.001).

Conclusions: The significant findings of our study underscore that in YOAD, despite more pronounced global impairment compared to LOAD, social cognition remains stable. This finding is crucial for understanding the patterns of social cognition in YOAD and may potentially guide future interventions and care strategies.