The fact that gender influences the immune system has long been recognised. The higher risk of women developing autoimmune diseases suggests that these are somehow mediated by sex steroids, with estrogens as enhancers at least of the humoral immunity and androgens and progesterone as natural immune-suppressors. The concept of immunosenescence reflects changes in both cellular and humoral immune responses. This may be related with the higher incidence of infectious and chronic diseases. Besides age, in postmenopausal women, changes of the immune system have been attributed to estrogen deprivation. There is an increase in pro-inflammatory serum markers, an increasing response of the body's cells to cytokines, a decrease in CD4 T and B lymphocytes and in the cytotoxic activity of NK cells. In fact IL-6 is a key factor in bone reabsorption by osteoclast activation and also seems to be associated with diseases that occur more in menopause such as diabetes, atherosclerosis and cardiovascular diseases. Recent studies indicate several changes in immune response, either with suspension of hormone therapy or with its replacement at menopause.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.2741/e190 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Drug Development.
Alzheimers Dement
December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
View Article and Find Full Text PDFBackground: Accumulating evidence suggests that the presynaptic protein α-synuclein (α-syn), is involved in the pathophysiology of AD and elevated in the cerebrospinal fluid (CSF). The role of Natural Killer (NK) cells of the innate immune system in AD has largely been overlooked. In a murine model, depletion of NK cells augmented the accumulation of pathological α-syn.
View Article and Find Full Text PDFDrug Development.
Alzheimers Dement
December 2024
Memory and Aging Center, UCSF Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Women account for almost two-thirds of Alzheimer's disease (AD) cases, yet evidence significantly less clinical benefit from recently deployed amyloid-lowering therapies. To close this disparity gap, there is an urgent need to identify biological drivers of sex differences in the manifestation and clinical response to AD therapeutics. A recent review of multi-omic studies of AD reported >75% of studies showed female-specific changes at the molecular level (vs.
View Article and Find Full Text PDFBackground: Evidence suggests glucagon-like peptide 1 receptor agonists (GLP-1RAs) may have therapeutic potential in Alzheimer's disease (AD). Cumulative evidence has indicated a potential reduction in cognitive decline in people with AD, while real-world evidence has shown decreased dementia risk in patients with type 2 diabetes. Non-clinical data reveal that GLP-1RAs impact neuroinflammation and other biological processes believed to be involved in AD pathophysiology, including effects on central and peripheral immune cells.
View Article and Find Full Text PDFBackground: Clinical assessments utilized in trials to measure progression in sporadic Alzheimer's disease (SAD) such as the MMSE, ADAS-Cog, CDR-SB and ADCS-ADL are well established. Distinct assessments are utilized for Down Syndrome-related Alzheimer's disease (DSAD). Although these assessments are less well established, they probe comparable domains of cognition and function.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!