Articles tagged with Alzheimer Disease
Researchers are working on finding elusive answers about Alzheimer's disease development. By leveraging computers and harnessing idle capacity, the project aims to accelerate research and uncover clues that could lead to a cure.
People with Alzheimer's experience a clear improvement in dementia-related behavior after visiting horses under supervision, with reduced fidgeting and resistance to care. The therapy boosts physical activity and lifts their mood, providing a unique way to ease symptoms without drugs.
Researchers found that Cajal-Retzius cell loss occurred with the onset and development of Alzheimer's disease, concomitant with amyloid pathology and behavioral deficits. The study, published in Neural Regeneration Research, used a mouse model to investigate the relationship between Cajal-Retzius cells and Alzheimer's disease.
Mayo Clinic researchers define a new subtype of Alzheimer's disease that produces different symptoms and affects the brain in unique ways. This subtype, called hippocampal sparing AD, may be misdiagnosed as other conditions, but could be treated with current medications.
A recent study used 7.0T magnetic resonance spectroscopy to analyze biochemical metabolism in the hippocampus of Alzheimer's disease rats. The findings revealed reduced N-acetylaspartate and elevated creatine and choline wave crests, indicating neuronal damage and inflammation.
Researchers find prion protein attaches to amyloid-beta peptides, contrary to previous studies, and do not break them down into smaller pieces. This discovery bodes well for a potential approach using prion-protein-based compounds to treat Alzheimer's disease.
A study published in Frontiers in Aging Neuroscience found that moderate physical activity can preserve the volume of the hippocampus in older adults at increased genetic risk for Alzheimer's disease. This suggests a potential delay in cognitive decline and onset of dementia symptoms.
Researchers have engineered a series of molecules with the potential to treat most neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's. The GAIM-changing molecules recognize characteristic common to many toxic misfolded proteins and can prevent new aggregates from forming while clearing existing ones.
Researchers identified a new class of compounds, called pharmacologic chaperones, that can increase retromer levels and decrease amyloid-beta levels in cultured hippocampal neurons. The study found these compounds to be relatively non-toxic and showed promise in treating neurologic disease.
A research team led by Dr. Zeng Li has discovered a novel function of the Amyloid Precursor Protein (APP), which controls the growth and maturation of newborn brain cells. This finding may help researchers understand how APP goes awry in Alzheimer's disease and potentially lead to innovative therapeutics.
Genetically modified neural stem cells have been shown to produce neprilysin, an enzyme that breaks down amyloid-beta, reducing its accumulation in the brain. The approach has shown promising results in two different mouse models, with a significant reduction in amyloid-beta plaques compared to controls.
Researchers found that carrying the ApoE4 gene variant increases the likelihood of developing mild cognitive impairment and Alzheimer's disease in women, but not in men. The discovery holds implications for genetic counselors and clinicians, and could shed light on the underlying causes of Alzheimer's disease.
Researchers have developed a new mouse model that accurately replicates the progression of Alzheimer's disease in humans. The models are characterized by early accumulation of Abeta peptides and cognitive dysfunction similar to human patients.
A study found that chronic cigarette smoking impairs postural stability in individuals with alcohol use disorders, even during sobriety. Non-smoking AD individuals improved on a measure of postural stability over eight months, while smoking AD individuals showed no significant improvement.
As the US population ages, Alzheimer's disease is projected to increase from 3 million in 2011 to over 10 million by 2050, affecting broad-based national policies. The annual cost of care for people over 70 is estimated at $157-$215 billion, with costs expected to reach $1.2-$1.6 trillion by 2040.
Researchers have found that caffeine can positively affect tau deposits in Alzheimer's disease, improving spatial memory and reducing pathogenic processes in genetically altered mice. The study suggests a new class of drugs may be developed for the treatment of Alzheimer's disease using an A2A antagonist.
African-Americans may be at a higher risk for developing Alzheimer's disease due to biologic and cultural factors. Researchers emphasize the need for increased participation of African-American participants in research studies to better understand the disease.
A new concept of Alzheimer's disease, as a spectrum of diseases, raises ethical and policy-related questions. Dr. Karlawish suggests preparing legal providers to assess decision-making ability and offering caregiver training to support those affected by the disease.
Researchers develop transgenic flies expressing anti-amyloid antibodies, which reduce neuronal loss and improve eye morphology. A second treatment involving secreted Heat shock protein 70 also shows protective effects, suggesting a new approach to targeting amyloids.
A non-invasive, rapid method for genotyping apolipoprotein E gene polymorphisms has been developed to help determine the role of the ε4 allele in neural regeneration in late-onset Alzheimer's disease cases. This method uses mouth swab specimens and real-time PCR, offering a safe and efficient alternative to traditional blood sampling.
Researchers found that Dab2 overexpression significantly increased TβRII and p-SMAD2/3 levels, reducing amyloid-beta deposition, microglia activation, and neuronal loss in APP/PS1 mouse brain tissue. This suggests a neuroprotective role of Dab2 in Alzheimer's disease.
Researchers have found that pramlintide reduces amyloid-beta peptides and improves learning and memory in Alzheimer's disease models. The study also suggests lower levels of amylin in blood among AD patients, which could lead to new diagnosis and treatment options.
Research reveals that lipid rafts are essential for the renewal of brain neurons in Alzheimer's disease by modulating the aberrant autophagic-lysosomal pathway. The study highlights a possible mechanism underlying the clearance of Alzheimer's disease products, implicating the autophagic-lysosomal pathway.
A smart home system, developed by Tecnalia, monitors a person's habits and activities to detect early symptoms of neurodegenerative diseases like Alzheimer's. The system records data from various sensors and identifies changes in behavior, allowing for early diagnosis and improved patient care.
Researchers at UTMB have discovered a way to remove the toxic oligomeric tau protein, which can slow down the progression of dementia caused by Alzheimer's disease. The treatment, TOMA antibody, protects brain cells from tau toxic aggregates and improves cognitive function.
Researchers have developed a new technology to detect misfolded protein fragments, known as Aβ oligomers, in cerebrospinal fluid that could lead to early diagnosis of Alzheimer's disease. The test showed high sensitivity and specificity, distinguishing between Alzheimer's patients and those with other neurodegenerative disorders.
Researchers are testing whether early medical intervention can slow down progression of Alzheimer's disease before symptoms emerge. The A4 trial involves enrolling individuals at risk for Alzheimer's, who will be told of their risk status and monitored for potential adverse reactions.
A new study reveals that REST, a gene regulator active during fetal brain development, switches back on later in life to protect aging neurons from various stresses. The researchers also showed that REST is lost in critical brain regions of people with Alzheimer's and mild cognitive impairment.
Studies suggest that eye structure and function may reveal features of early-stage Alzheimer's disease, including changes in retinal pigment epithelial layer and choroidal layer thickness. Researchers hope to develop new diagnostic methods using the eye as a window to brain activity.
Researchers have found a way to slow down the formation of amyloid plaques, a hallmark of Alzheimer's disease, by rescuing the Golgi structure in cells. By inhibiting an enzyme or expressing a mutant protein, the researchers were able to decrease harmful Abeta secretion by 80 percent.
A team of scientists has discovered a new therapeutic target for Alzheimer's disease by blocking the production of key neurotoxic peptides linked to the condition. The drug candidate, E64d, has been shown to be safe in humans and has improved memory deficits in mouse models.
Researchers at Temple University found that chronic sleep disturbance can trigger the onset of Alzheimer's disease. The study used a transgenic mouse model to show that sleep deprivation impairs memory and tau metabolism, leading to accelerated brain pathology.
Researchers detected early evidence of Alzheimer's disease using brain scans and found that those with positive scans had a faster rate of decline on memory, language, and reasoning over three years. This biomarker could help clinicians better evaluate and treat patients at risk for cognitive decline.
A midlife healthy diet was found to reduce dementia risk by almost 90% compared to the least healthy diet. Higher intake of saturated fats linked to poorer cognitive functions and increased risk of dementia.
Researchers uncover an entire network of cellular helpers to mitigate damage, identifying new regulatory mechanisms for the heat shock response. The study's findings may also offer insights into neurodegenerative diseases such as Alzheimer's and Parkinson's.
Researchers have discovered a blood test that can predict cognitive decline and Alzheimer's disease within three years with greater than 90 percent accuracy. The test identifies 10 lipids in the blood, which appear to reveal the breakdown of neural cell membranes in participants who develop symptoms.
Margaret Cheung, a UH physicist, has been awarded the American Physical Society fellowship for her work on biophysics and its applications to cancer and Alzheimer's research. Her research focuses on understanding protein behavior in cells to develop novel therapeutic strategies.
Researchers have found that rapid neuronal damage occurs 10-20 years before symptoms of inherited Alzheimer's disease appear, providing a crucial window for intervention. A clinical trial is underway to test the safety and efficacy of experimental drugs in this population.
A team of researchers at Brigham and Women's Hospital has generated stem cells from skin biopsies of living family members with a genetic predisposition to early-onset Alzheimer's. The study found that the APPV7171 mutation alters amyloid-beta protein generation, Tau protein expression, and phosphorylation, providing new insights into ...
A new study suggests that Alzheimer's disease contributes to nearly as many deaths in the United States as heart disease or cancer. Researchers analyzed data from 2,566 participants aged 65 and older, finding a significant association between dementia diagnosis and increased mortality.
Researchers at Washington University School of Medicine found that biomarkers of neuronal injury in Alzheimer's disease decrease as symptoms of dementia appear, contrary to previous findings. This reversal suggests a slowing of cell death and may be an important criterion for assessing the success of treatment trials.
Researchers at Harvard University have successfully converted patient skin cells into human brain cells, offering a new model for studying and developing treatments for early-onset Alzheimer's disease. The study found that preventing amyloid-beta imbalances can reduce levels of distorted tau protein.
A yeast model of Alzheimer's disease has identified a drug candidate, clioquinol, that reduces amyloid-β levels by 90% and restores cellular protein-trafficking. The mechanism of action involves chelating copper, which makes Aβ more toxic.
Researchers found that twin brains with identical diagnoses showed similar combinations of pathologies, including damage to two or more areas of the brain. This study provides evidence that there may not be a single cause of Alzheimer's, but rather multiple factors contributing to its development.
Researchers found that Alzheimer's disease disrupts the biological clock in fruit flies, causing irregular sleep-wake patterns. The study suggests that the biological clock is still ticking but being ignored by other parts of the brain and body.
New research from Washington University School of Medicine finds that increased brain cell activity boosts brain fluid levels of tau protein, a hallmark of Alzheimer's disease. The study suggests that brain cells may be secreting tau when they send signals, potentially leading to the spread of disease.
A new gene has been isolated that plays a causal role in the development of Alzheimer's disease. The gene affects amyloid-beta protein accumulation, leading to brain damage and disease progression. This breakthrough could lead to new avenues for therapeutic design and early detection methods.
A recent study by Erin Abner, Ph.D., found that subjective memory complaints can be predictive of clinical memory impairment. The results are encouraging as they might help identify people at risk of developing Alzheimer's Disease sooner.
A multi-site US-Canada study found that antidepressant citalopram significantly relieved symptoms of agitation in Alzheimer's patients and reduced caregivers' stress levels. The study involved 186 patients with Alzheimer's disease who showed no relief from non-medication therapies or antipsychotic drugs.
A study found that citalopram reduced agitation in Alzheimer's patients, but at the cost of mild cognitive impairment and increased risk of cardiac adverse effects. The researchers concluded that citalopram cannot be generally recommended as an alternative treatment option due to its limitations.
A high dose of antidepressant citalopram significantly reduced agitation in Alzheimer's patients, but higher doses pose a risk of heart rhythm disorder. Caregivers experienced reduced distress when caring for patients taking the medication.
A clinical trial found that antidepressant citalopram significantly relieved agitation in patients with Alzheimer's disease, with 40% of patients experiencing considerable relief. However, the drug also had decreased cognitive function and longer QTc intervals, a measure of abnormal heart function.
Researchers are exploring the properties of amyloid beta peptides, implicated in Alzheimer's disease. By understanding their behavior, they hope to identify structures that lead to toxic aggregates and develop treatments.
Researchers at the University of Southampton have discovered a key role for astrocytes and specific proteins in supporting neurons during protein misfolding brain diseases. The study found that certain proteins increase in response to misfolded proteins, potentially providing protection against neuronal death.
Research from Karolinska Institutet reveals lower levels of resolution-regulating molecules in Alzheimer's patients' brains and cerebrospinal fluid, correlating with reduced cognitive function. The study suggests stimulating inflammation resolution may prevent neuronal death and improve memory functions.
A study found that people with both parents having Alzheimer's disease showed more severe brain abnormalities, including increased brain plaques and reduced brain volume. The research suggests a possible genetic link to the development of Alzheimer's disease.
Researchers at Rutgers University–Camden studied microRNAs in common fruit flies to understand the connection between aging and diseases like Alzheimer's. They found that as fruit flies age, more microRNAs accumulate on a protein complex, impacting age-associated events and leading to shorter lifespans.
Cedars-Sinai researchers found that genetically targeting immune cells to overproduce ACE breaks down beta-amyloid plaque, preventing cognitive decline in laboratory mice. The study identifies a novel role for ACE in the clearance of beta-amyloid in brain blood vessels.
A study published in Nature Neuroscience suggests that abnormal gene expression resulting from DNA relaxation can be detected in the brain and blood of Alzheimer's patients. The researchers propose that drugs modifying DNA structure may be beneficial for treating Alzheimer's disease, paving the way for epigenetic-based therapies.
A study at UT Southwestern Medical Center found elevated levels of DDT metabolite DDE in patients with Alzheimer's, suggesting a link between DDT exposure and the disease. The study suggests that early biomarkers could help predict Alzheimer's development due to DDT exposure.