Background: Dietary acid load (DAL) has been associated with frailty and hip fractures in older adults, who often have a reduced kidney function and thus compromised buffering capacities. Studies to quantify DAL in older adults are scarce and controversies persist as to whether DAL in- or decreases with age.
Aim: To enhance the understanding of DAL in older individuals, we examined its relationship with increasing age and selected anthropometric data in a well-characterized sample of US adults.
Methods: Secondary data analysis of nationally representative data from the National Health and Nutrition Examination Surveys data (NHANES 2011-2016). The sample included n = 3018 adults aged 60+, which may be extrapolated to represent n = 45,113,471 Americans. DAL was estimated using 4 formulas, including Potential Renal Acid Load (PRAL) and Net Endogenous Acid Production (NEAP).
Results: All employed DAL scores tended to decline with increasing age. Participants aged 80 years or older yielded the lowest DAL scores. The average US citizen aged 60+ consumed an acidifying diet, yet there were sex-specific differences in the adjusted means for some scores. NEAP was positively correlated with both body mass index (r = 0.26, p < 0.001) and the sagittal abdominal diameter (r = 0.31, p < 0.001) in this nationally representative sample.
Conclusion: The previously reported phenomenon of increasing DAL values in older people in non-Western countries may not apply to the US. Our findings may constitute an important step towards a better understanding of DAL in older US adults, and highlight the need for additional population-specific research in the field.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10519865 | PMC |
http://dx.doi.org/10.1007/s40520-023-02508-6 | DOI Listing |
Background: Microglia are the primary immune cells of the brain and represent the main line of defense against brain environmental insults. In recent years, microglia have been implicated in Alzheimer's disease (AD) pathogenesis by having interconnected yet opposing roles: beneficial as they clear amyloid beta (Aβ) and amyloid plaques, and detrimental as being responsible for synaptic and neuronal loss. These activities are tightly regulated by microglia receptors CD33 and TREM2.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
CEDOC - Nova Medical School - Universidade NOVA de Lisboa, Lisboa, Portugal.
Background: Alzheimer's disease (AD), an untreatable synaptic disorder, is the most frequent cause of dementia. It is still unclear which mechanisms drive the early synapse dysfunction in the most common late-onset AD (LOAD). The second most important LOAD risk gene identified, BIN1, is an endocytic regulator.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Byrd Alzheimer's Center & Research Institute, Tampa, FL, USA.
Background: Microglia play significant roles in Alzheimer's disease (AD) pathophysiology. Current evidence suggests microglia may function in both protective and degenerative capacities, which has received little clarity from transcriptionally-characterised phenotypes uncovered from transgenic pathologies alone. BIN1 - the second-most significant risk gene for the development of late-onset AD (LOAD) - is expressed at high levels in neurons, oligodendrocytes and microglia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, New Orleans, LA, USA.
Background: Increasing evidence suggests that SARS-CoV-2 infection may lead to early onset and aggravation of pre-existing vascular dementia and Alzheimer's disease. Methylene tetrahydrofolate reductase (Mthfr) is a critical enzyme in folate metabolism, also required for optimal brain function. Mthfr deficient mice display cognitive impairments and neurovascular deficits and polymorphisms in MTHFR increases dementia risk.
View Article and Find Full Text PDFBackground: Many putative factors may contribute to the neurodegeneration seen in Alzheimer's Disease (AD), including the build-up of toxic amyloid-beta plaques and the aberrant reactivity of non-neuronal cell types such as astrocytes and microglia. However, the precise contribution of these factors to normal and disease states of neurons remains poorly defined.
Method: We employed in vitro rat neural co-culture models to determine how changes in cell interactions alter the transcriptional response of neural cell types to agents associated with neurodegeneration.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!