Ageing research reviews最新文献

Aging brings with it many health issues that can make life challenging. As much of the attention is given to non-communicable diseases, there are others which are slowly becoming a matter of great concern. One such issue is cognitive frailty, which is a high risk factor for dementia, falls, fractures and hospitalization. Though not yet declared a public health concern, it deserves early detection and prevention strategies. As it is reversible if treated on time, there is a need to look into its prevention and cure. Physical activity has proven to be very effective in the treatment of cognitive frailty. This scoping review thus aims to study the impact of physical activity through social participation on cognitive frailty. The authors recommend that focussing on one's muscular fitness through participation in sports and elements of Indian classical dance form like Kathak in groups/ communities can be a very effective way of combating cognitive frailty among older adults.

Endothelial colony-forming cells (ECFCs), a unique endothelial progenitor subset, are essential for vascular integrity and repair, providing significant regenerative potential. Recent studies highlight their role in cerebrovascular aging, particularly in the pathogenesis of vascular cognitive impairment and dementia (VCID). Aging disrupts ECFC functionality through mechanisms such as oxidative stress, chronic inflammation, and cellular senescence, leading to compromised vascular repair and reduced neurovascular resilience. ECFCs influence key cerebrovascular processes, including neurovascular coupling (NVC), blood-brain barrier (BBB) integrity, and vascular regeneration, which are critical for cognitive health. Age-related decline in ECFC quantity and functionality contributes to vascular rarefaction, diminished cerebral blood flow (CBF), and BBB permeability-processes that collectively exacerbate cognitive decline. This review delves into the multifaceted role of ECFCs in cerebrovascular aging and underscores their potential as therapeutic targets in addressing age-related vascular dysfunctions, presenting new directions for mitigating the effects of aging on brain health.

Mild behavioral impairment (MBI) represents a recently introduced diagnostic concept that focuses on behavioral and personality changes occurring in late life and associated with cognitive decline. Nevertheless, the relationship between these dimensions remains unclear. This systematic review and meta-analysis aim to analyze the relationship between MBI and cognitive functioning. The review process was conducted according to the PRISMA-Statement. Restrictions were made, selecting the studies published in peer-review journals, including at least one cognitive measure and presenting the measurement of MBI. Studies that included participants with neurological disorders, dementia, or psychiatric disorders or that only did a neuroimaging or genetic study were excluded. Twenty-two studies were included in the systematic review, while in the meta-analysis seventeen studies featured data to be included in the analyses. The results were classified according to the following cognitive domains: global cognitive functioning, memory, language, attention executive functions, visuospatial skills, and processing speed. In the quantitative analysis, only global cognitive functioning, executive function, attention, and memory were evaluated. The results of both qualitative and quantitative analysis indicate that individuals with MBI exhibited diminished performance on cognitive tasks when compared to those without MBI symptoms. These results are stronger when evaluating the various domains individually (particularly memory and executive functions) than when a global assessment was made. These findings highlight the potential role of MBI symptoms as early indicators of neurodegenerative processes, reinforcing the necessity for comprehensive assessments that encompass both behavioral and cognitive evaluations. The early detection of these symptoms in prodromal phases can be very useful for the development of non-pharmacological interventions and may provide relevant guidelines for clinicians in the management and diagnosis of neurodegenerative disorders.

Alzheimer's disease (AD), an age-related neurodegenerative disease, brings huge damage to the society, to the whole family and even to the patient himself. However, until now, the etiological factor of AD is still unknown and there is no effective treatment for it. Massive deposition of amyloid-beta peptide(Aβ) and hyperphosphorylation of Tau proteins are acknowledged pathological features of AD. Recent studies have revealed that neuroinflammation plays a pivotal role in the pathology of AD. With the rise of nanomaterials in the biomedical field, researchers are exploring how the unique properties of these materials can be leveraged to develop effective treatments for AD. This article has summarized the influence of neuroinflammation in AD, the design of nanoplatforms, and the current research status and inadequacy of nanomaterials in improving neuroinflammation in AD.

Protein lactylation, an emerging post-translational modification, is providing new insights into tumor biology and challenging our current understanding of cancer mechanisms. Our review illuminates the intricate roles of lactylation in carcinogenesis, tumor progression, and therapeutic responses, positioning it as a critical linchpin connecting metabolic reprogramming, epigenetic modulation, and treatment outcomes. We provide an in-depth analysis of lactylation's molecular mechanisms and its far-reaching impact on cell cycle regulation, immune evasion strategies, and therapeutic resistance within the complex tumor microenvironment. Notably, this review dissects the paradoxical nature of lactylation in cancer immunotherapy and radiotherapy. While heightened lactylation can foster immune suppression and radioresistance, strategically targeting lactylation cascades opens innovative avenues for amplifying the efficacy of current treatment paradigms. We critically evaluate lactylation's potential as a robust diagnostic and prognostic biomarker and explore frontier therapeutic approaches targeting lactylation. The synergistic integration of multi-omics data and artificial intelligence in lactylation research is catalyzing significant strides towards personalized cancer management. This review not only consolidates current knowledge but also charts a course for future investigations. Key research imperatives include deciphering tumor-specific lactylation signatures, optimizing synergistic strategies combining lactylation modulation with immune checkpoint inhibitors and radiotherapy, and comprehensively assessing the long-term physiological implications of lactylation intervention. As our understanding of lactylation's pivotal role in tumor biology continues to evolve, this burgeoning field promises to usher in transformative advancements in cancer diagnosis, treatment modalitie.

Objective: the ε4 allele of the apolipoprotein E gene (APOE4) is recognized as the primary genetic risk factor for Alzheimer's disease (AD) and has been associated with chronic inflammatory conditions, such as periodontal disease (PD). PD has been identified as having a potentiating effect that favors the development and progression of AD. This scoping review investigates the potential relationship between PD and AD through APOE4 METHODS: the Joanna Briggs Institute methodology was used. The search included articles published in PubMed and Embase, focusing on human studies, and excluding case series, in vitro studies, reviews, and animal studies.

Results: among the studies that evaluated the relationship between PD, APOE4, and AD, a correlation was identified between the gingival index and cognitive impairment in APOΕ4 carriers. Additionally, higher levels of apolipoprotein E4 were found in the crevicular fluid of patients with both AD and PD, compared to individuals without AD.

Conclusion: APOE4 may link PD and AD through shared genetic variants, inflammatory pathways, and dyslipidemia, involving both peripheral and central pathways. More comprehensive studies are required to ascertain the relationship between PD, AD, and APOE4 more accurately, and to clarify whether these connections are causal or non-causal.

Mitochondrial dysfunction and oxidative stress are critical factors in the pathogenesis of neurodegenerative diseases. The complex interplay between these factors exacerbates neuronal damage and accelerates disease progression. In neurodegenerative diseases, mitochondrial dysfunction impairs ATP production and promotes the generation of reactive oxygen species (ROS). The accumulation of ROS further damages mitochondrial DNA, proteins, and lipids, creating a vicious cycle of oxidative stress and mitochondrial impairment. This review aims to elucidate the mechanisms by which mitochondrial dysfunction and oxidative stress lead to neurodegeneration, and to highlight potential therapeutic targets to mitigate their harmful effects.

Background: Presently, colorectal cancer (CRC) is the second leading cause of cancer-related deaths worldwide. We provided global, regional, and national estimates of the burden of CRC and their attributable risks from 1990 to 2021, aiming to guide screening, early detection, and treatment strategies, optimize healthcare resource allocation, and facilitate the rational management of burden of CRC.

Methods: Using data derived from the Global Burden of Disease database, we estimated the incidence, mortality, and disability-adjusted life years (DALYs) of CRC. The temporal trends of the age-standardized rate of CRC were quantified by calculating the estimated annual percentage changes (EAPC). Deaths from CRC attributable to each risk factor that had evidence of causation with CRC were estimated. CRC's deaths and DALYs was forecast through 2050 by logistic regression with Socio-Demographic Index as a predictor, then multiplying by projected population estimates.

Results: Globally, between 1990 and 2021, the incident cases, death cases, and DALYs attributed to CRC have doubled, the age-standardized incidence rate (ASIR) presented a slightly upward tendency, while the age-standardized death rate (ASMR) and the age-standardized DALYs rate (ASDR) exhibited a decreasing trend. From 1990-2021, the ASIR for males has an increased trend, while females presented a downward trend. The ASIR and ASDR of CRC were higher in high and high-middle sociodemographic index (SDI) countries. The ASIR of CRC in 165 countries and territories showed escalating trend. Globally, for males and both sexes combined, diet low in whole grains was the leading risk factor for age-standardized deaths from CRC in 2021. However, among females, diet low in milk was the leading risk factor. We forecast that 2.18 million (1.53-2.94) individuals will death for CRC worldwide by 2050, and the DALYs achieve 41.7 million (29.9-55.4) by 2050.

Conclusion: The doubling of incidence counts and mortality cases and the rising ASIR in most countries indicates a significant burden of CRC. Authorities should devise suitable measures to address the increasing burdens, such as optimizing screening programs, enhancing awareness and screening efforts for males, and reducing exposure to modifiable risk factors.

Alzheimer's Disease (AD) is a major global health challenge, largely due to its complex pathology and the limited effectiveness of existing treatments. Quercetin, a bioactive compound belonging to the flavonoid class, its promising antioxidant, anti-inflammatory, and neuroprotective effects in addressing AD. However, its therapeutic potential is hindered by challenges such as low bioavailability, instability, and restricted permeability across the blood-brain barrier (BBB). Advances in nanotechnology have paved the way for quercetin-functionalized nanomaterials, offering solutions to these challenges. These nanostructures enhance quercetin's solubility, stability, and targeted brain delivery, thereby augmenting its therapeutic potential. In this review, nanocarriers (like liposomes, polymeric nanoparticles, and metal-based nanosystems) are explored for their potential application in optimizing quercetin delivery in AD management. It discusses the mechanisms by which these nanostructures enhance BBB penetration and exert neuroprotective effects. Furthermore, the review examines the outcomes of preclinical and in vitro studies, while addressing the challenges of scaling these approaches for clinical application. By merging the fields of nanotechnology and neurotherapeutics, the importance of quercetin-functionalized nanomaterials in advancing AD management strategies is underscored in this review.

Sarcopenia refers to a neuromuscular disease characterized by age-related declines in muscle mass and function. Since Professor Rosenberg first introduced the concept of sarcopenia in 1989, numerous operational paradigms have been proposed, tested, and validated against negative outcomes. The most recent recommendations advocate that dynapenia, or reduced of muscle strength, should be used alongside low muscle mass for the identification of sarcopenia. This approach is based on the understanding that impairments in muscle strength are a major consequence of muscle failure. However, empirical evidence has yielded conflicting results regarding the ability of current sarcopenia definitions to identify individuals at higher risk of adverse health-related events. Muscle power - the capacity to generate strength rapidly - has emerged as a critical domain of physical performance in old age. Not only does it decline earlier and more drastically than other measures (e.g., muscle strength), but it is also more strongly associated with adverse outcomes. In this view point, we provide an appraisal of muscle power as a more reliable indicator of muscle failure, compared with other measures (e.g., strength), for identifying individuals with sarcopenia in both geriatric and non-geriatric settings. We also discuss major challenges hindering the conduct of meaningful investigations on this subject.