Articles tagged with Alzheimer Disease
Gene replacement in pigs alleviates intestinal obstruction associated with cystic fibrosis. In contrast, Alzheimer's disease is characterized by the removal of synaptic protein ADAM10. These findings provide insight into pathophysiology and suggest tissue-specific gene replacement can alleviate CF symptoms.
Scientists have reevaluated the role of the APOE gene in Alzheimer's disease, finding minimal interaction between APOE and amyloid beta in cerebrospinal fluid. This suggests a need to rethink therapeutic strategies targeting APOE, as current approaches may not be effective.
A cross-sectional study of 1,870 individuals found that long-lived families have a reduced risk of cognitive impairment consistent with Alzheimer's disease. The study suggests a delayed onset of disease in these families, protecting their members but not later in life.
Researchers have identified nine biomarkers associated with the buildup of toxic protein amyloid beta in the brain, which occurs years before symptoms appear. The discovery has the potential to lead to the development of an early screening test for Alzheimer's disease, giving those at risk a better chance of receiving treatment earlier.
Researchers discovered a protective CD33 gene variant that enhances the brain's immune system to clear away toxic A-beta protein, a hallmark of Alzheimer's disease. This finding raises the possibility of using CD33 inhibitors as a potential new approach to treating and preventing Alzheimer's.
Researchers identified a network of genes involved in inflammatory response driving Late Onset Alzheimer's Disease (LOAD), providing new understanding of key pathways and genes. The study suggests targeting the TREM2-TYROBP pathway as potential therapies for LOAD.
A study published in the journal Neuron reveals that a gene called CD33 contributes to Alzheimer's disease by inhibiting immune cells' ability to remove toxic molecules. Inactivation of CD33 has been shown to enhance microglia's clearance of beta-amyloid plaques, potentially reversing the disease's progression.
Researchers analyzed 1,647 brain tissue samples to identify molecular networks disrupted in Alzheimer's disease, highlighting the crucial role of TYROBP in immune system dysfunction. This study provides a new framework for understanding Alzheimer's mechanisms and developing potential therapies.
Case Western Reserve University spinoff ReXceptor has secured $1.4 million to advance its novel Alzheimer's treatment strategy. The company plans to initiate early-stage human clinical trials using bexarotene, a medication that significantly clears amyloid beta in mice.
A NIH-funded study has discovered a potential strategy for treating Alzheimer's disease by blocking the activity of a little-known regulator protein called CD33. The study found that CD33 promotes late-onset Alzheimer's by preventing support cells from clearing out toxic plaques.
A study published in PNAS reveals how disrupted cellular energy metabolism contributes to the development of Alzheimer's disease. In early-stage Alzheimer's, amyloid-beta-peptide accumulation disrupts mitochondrial function, leading to over-accumulation of calcium and neuronal death.
Researchers have found that high-frequency bursts in the brain improve the ratio of healthy amyloid-beta 40 to unhealthy 42, potentially protecting against Alzheimer's. The study suggests environmental changes and experiences can modify synapse properties, leading to increased production of amyloid-beta 40.
Researchers at Duke University Medical Center found that close family members of people with Alzheimer's disease are more likely to develop silent buildup of brain plaques associated with the disease. The study suggests unidentified genetic factors may influence the development of Alzheimer's before dementia onset.
A new study finds that the US is facing a severe neurologist shortage, with a projected need for 11% more doctors to meet current needs by 2025. The demand for neurologists is expected to grow faster than the supply, with average wait times for new and follow-up visits increasing.
Researchers discovered that high cholesterol levels can cause defective cell division, leading to Alzheimer's disease and atherosclerosis. Cholesterol disrupts the process of cell division, resulting in cells with incorrect numbers of chromosomes and genes.
Researchers found that the APOE gene and ABCA7 gene were significant risk factors for late-onset Alzheimer's disease in African Americans. The study also suggests that these genes may be shared with Caucasians, but with different variants. Further studies are needed to understand the biologic implications of these findings.
Researchers have shed light on microglial cells in Alzheimer's patients, finding they lose two biological functions as the disease progresses. The study suggests beta-amyloid peptides trigger this process, and reversing microglial function could lead to treatments for the disease.
A new hypothesis suggests that spherical structures in the nucleus, containing FE65 and BLM proteins, can give a wrong signal for cell division. This degeneration and death of nerve cells is linked to Alzheimer's patients.
The American College of Physicians has developed interventions to help patients with prediabetes, gout, obesity, and Alzheimer's disease. The organization has created patient guides and videos that provide practical tips and concrete examples for reducing the risk of developing diabetes, managing gout, and achieving healthy weight loss.
Researchers have discovered that brain damage in Alzheimer's disease is caused by the overactivation of an enzyme called AMPK, leading to the loss of synapses and neuron damage. Blocking this enzyme in mouse models prevented further neuronal loss.
Researchers have created a new genetically engineered rat model that closely represents the brain changes associated with Alzheimer's disease, including tau pathology and extensive neuronal cell death. The rats developed memory and learning problems with age, supporting the idea that increases in beta-amyloid causes the disease.
African-Americans with a variant of the ABCA7 gene have nearly double the risk of developing late-onset Alzheimer's disease compared to those without the variant. The study, led by Columbia University Medical Center, suggests that lipid metabolism may play a more important role in Alzheimer's disease among African-Americans.
A study published in JAMA Network identifies genetic variants associated with Alzheimer's disease in African Americans, including ABCA7 and APOE genes. The findings suggest that these variants may also be relevant for individuals of European ancestry.
A study found a significant association between the ABCA7 gene variation and increased late-onset Alzheimer disease risk among African Americans, with a twofold increase in risk compared to European American populations. The research also highlights unique genetic risk levels for African Americans.
Scientists have identified several genes linked to the tau protein, which is found in brain tangles that develop in Alzheimer's patients. The findings may help provide targets for a different class of drugs that could be used for treatment.
A new study has identified genetic markers that may signal individuals at increased risk of developing Alzheimer's disease. The research found mutations in certain genes influencing protein accumulations in the brain and spinal fluid, which can lead to cognitive decline.
A new study estimates that dementia care costs are comparable to those of heart disease and cancer, with annual costs ranging from $159-$215 billion. The majority of these costs are due to long-term daily care and supervision provided by families and nursing homes.
Researchers at the New York Stem Cell Foundation have developed a 3D stem cell culture technique to study Alzheimer's disease. This technique enables the creation of neuron aggregates that can be used to model and study diseases such as Alzheimer's and Parkinson's.
Women who undergo surgical menopause experience a two-fold increase in cognitive decline and dementia due to premature estrogen loss. Research suggests that this leads to increased sensitivity to stressors and abnormal protein production, which can contribute to Alzheimer's disease. Follow-up studies are needed to confirm the findings.
Researchers at Mount Sinai Hospital are collaborating with the New York Stem Cell Foundation to use stem cells to gain a better understanding of Alzheimer's disease. The project aims to identify causes and cures for the common form of AD, using reprogrammed skin cells into brain cells.
Researchers found that long-term treatment with carmustine decreased amyloid beta levels by 75% in a mouse model of Alzheimer's disease. Carmustine, a cancer treatment, shows promise as a potential drug for reducing Alzheimer's symptoms.
Researchers at Gladstone Institutes found that a certain type of DNA damage can occur during normal brain functions such as learning. The team identified two therapeutic strategies that reduce disruptions to this process, which is associated with Alzheimer's disease.
A Mayo Clinic study found that men with dementia with Lewy bodies are five times more likely to have rapid eye movement (REM) sleep behavior disorder, which can appear decades before a diagnosis. The study suggests that screening for this sleep disorder could improve diagnosis and treatment of dementia with Lewy bodies.
A study found that extra virgin olive oil's oleocanthal can boost production of proteins and enzymes involved in removing beta-amyloid from the brain, potentially reducing Alzheimer's risk.
A study by Columbia University Medical Center researchers found that depression and cognitive status are independently associated with a more rapid decline in everyday living abilities. The findings suggest providing mental health treatment may slow the loss of independence.
AgedBrainSYSBIO assembles 14 international research teams to tackle ageing and cognitive decline using GWAS, comparative genomics, and protein-protein interactions. The project aims to identify druggable targets for preventing and curing age-related diseases.
A recent study published in JAMA Neurology found that unmedicated adults with hypertension and a genetic risk factor for Alzheimer's disease have higher amyloid plaque levels than other groups. Controlling hypertension may significantly decrease the risk of developing amyloid deposits, even in those with genetic risk.
A new tau transmission model opens doors for potential treatments of Alzheimer's and Parkinson's diseases by inducing animal models to mimic the spread of tau pathology. The research demonstrates cell-to-cell transmission of neurodegenerative proteins, offering therapeutic opportunities.
Researchers at Case Western Reserve University found that normal prion protein PrPc plays a crucial role in regulating iron metabolism, which may contribute to neuronal death in CJD. Iron imbalance caused by prion aggregation leads to neurotoxicity and brain cell death.
A phase IIa study suggests that ORM-12741, a new add-on drug, improves memory scores by 4% in individuals with moderate Alzheimer's disease, while worsening it by 33% in those receiving a placebo. The study found significant benefits in improving brain functions under stressful conditions.
Researchers found that participants with preclinical Alzheimer's disease had poorer sleep efficiency and spent less time asleep than those without markers of the disease. Early evidence suggests a possible connection between sleep loss and brain plaques, a hallmark of Alzheimer's disease.
Researchers at Rush University Medical Center found that buphenyl increases beneficial proteins in the brain, protects neurons, and improves memory and learning in mice with AD-like pathology. The study offers a promising avenue for treating Alzheimer's disease.
Researchers at University of British Columbia have found that blood vessels in the brain can be normalized with amyloid beta immunization, reducing plaque build-up and brain capillary growth. This discovery suggests that drugs targeting blood vessels could be effective in treating Alzheimer's disease.
Researchers have developed a new approach to screening potential treatments for Alzheimer's disease using the C. elegans worm model. The study identified six compounds capable of alleviating tau-induced behavioral abnormalities in the worm model, as well as azaperone treatment, which can decrease abnormal tau accumulation.
A new study found that prolonged exposure to an enriched environment activates brain receptors, preventing amyloid beta protein from weakening nerve cell communication. This provides a molecular mechanism for why a richer environment can help lessen the memory-eroding effects of Alzheimer's disease.
A new protein, CALHM1, has been identified as a key regulator of the sense of taste. The discovery, made by Philippe Marambaud at the Feinstein Institute for Medical Research, sheds light on the mechanisms of communication between the brain and the senses.
Researchers at the University of Michigan have discovered that green tea extract can prevent the misfolding of specific proteins in the brain, which is associated with Alzheimer's disease. The study found that a molecule in green tea, EGCG, prevented aggregate formation and broke down existing structures in proteins containing metals.
UCLA researchers found a common abnormality in genetic code that increases Alzheimer's risk, weakening brain connections. The study combined genomic screening with advanced brain scans to pinpoint the SPON1 gene as a culprit.
A new trial will test whether losartan, a widely used high blood pressure medication, can slow the progression of Alzheimer's disease. The RADAR clinical trial aims to improve brain blood flow and alter chemical pathways that cause brain cell damage.
Using both familial and sporadic AD iPSCs, the researchers discovered that pathogenesis differed between individual AD patients. They found stress phenotypes associated with intracellular amyloid beta oligomers and attenuated these phenotypes with docosahexaenoic acid (DHA) treatment.
Researchers have identified a key molecular system responsible for the inflammatory reaction in Alzheimer's disease. Signalling through CSF1R receptor is crucial for microglial population expansion, and targeting this pathway with selective inhibitors may delay clinical symptoms.
Researchers have discovered how methylene blue modifies tau proteins, which aggregate in Alzheimer's disease. The study reveals that methylene blue deactivates molecular residues promoting bonding and acts as a spacer to keep proteins apart, leading to potential treatment strategies.
A new study reveals that slow-firing neurons are essential for higher-order thinking and mental representations, which are compromised in diseases like schizophrenia and Alzheimer's. The research identifies NMDA-NR2B receptors as key regulators of neuronal firing.
A recent genome-wide imaging study has discovered a new gene, BCHE, associated with Alzheimer's plaques. The study found that variants of the BCHE gene are significantly linked to increased levels of amyloid plaque deposits in the brains of patients and those at risk for the disease.
Researchers at UC San Diego found that glutamate binding to NMDA receptors causes conformational changes leading to weakened synapses and impaired brain function. Beta amyloid peptide also weakens synapses by causing similar conformational changes.
Researchers found that white matter hyperintensities (WMHs) are equally associated with an Alzheimer's diagnosis as amyloid plaque. WMHs were also predictive of which subjects with mild cognitive impairment would go on to develop Alzheimer's. The study suggests potential ways to prevent Alzheimer's in those with amyloid deposits.
Researchers found that tetrahydroxystilbene glucoside (TSG) reverses α-synuclein overexpression and accumulation in a mouse model of Alzheimer's disease. The study suggests TSG may have therapeutic potential for preventing and treating AD.
Mice with Alzheimer's-like pathologies showed improved memory and slower disease progression on a low-protein diet supplemented with specific amino acids. The study found reduced levels of IGF-1 and increased blockade of its effects, suggesting potential non-invasive treatments.
A study by UC Davis researchers found that vascular brain injury, not amyloid plaques, has the greatest impact on cognitive domains. Vascular brain injury was associated with worse memory and executive function, while amyloid deposition had little to no effect.
A new study projects that Alzheimer's disease cases will increase from 4.7 million in 2010 to 13.8 million in 2050, with 7 million cases expected in people aged 85 or older. The increasing number of dementia cases poses a significant burden on society and highlights the need for more research, treatments, and preventive strategies.