Articles tagged with Alzheimer Disease
Researchers found a strong association between elevated pulse pressure and an increased risk of cerebrovascular disease in Alzheimer's patients. The study suggests that targeting the pulsatile component of blood pressure may offer new treatment implications for Alzheimer's patients.
Researchers discovered a new gene, SORL1, associated with early-onset forms of Alzheimer's disease. Mutations in this gene may contribute to the development of the disease by increasing beta-amyloid peptide production.
Scientists at Gladstone Institutes discover apoE protein plays distinct roles in young and aging brains, suggesting new research avenues for treating Alzheimer's. Increased ApoE levels can damage brains later in life, challenging current thinking.
A cholesterol drug commonly prescribed to reduce cardiovascular disease risk restores blood vessel function in a mouse model of Alzheimer's disease. The drug also improves learning and memory in adult mice, but not aged mice.
Researchers found a decrease in cerebrospinal fluid biomarker P-tau following treatment with bapineuzumab, suggesting potential benefits for Alzheimer's patients. However, further examination is needed to determine if these changes correlate with clinical improvements.
BIDMC researchers create novel antibodies that distinguish between healthy and disease-causing tau isoforms, raising the possibility of an immunization strategy for early-stage Alzheimer's diagnosis and treatment. The findings also suggest that targeting only the disease-causing isoform could prevent or slow disease progression.
Researchers at the University of California, San Diego, found that chronic stress triggers the production and accumulation of insoluble tau protein aggregates inside brain cells, similar to neurofibrillary tangles. This may explain why people prone to stress are more likely to develop sporadic Alzheimer's disease.
A meta-analysis of 13 studies found a significant association between lower Aβ42: Aβ40 ratios and development of Alzheimer disease and dementia. The analysis suggests that measuring this ratio may have value in predicting the risk for later development of dementia or AD.
A new study finds that brain insulin resistance contributes to cognitive decline in Alzheimer's disease, independent of diabetes status. Insulin-sensitizing medicines may have therapeutic potential to correct insulin resistance and slow down or improve cognitive decline.
Researchers found that Alzheimer's disease and other dementias spread within nerve networks by moving directly between connected neurons. The study used magnetic resonance imaging research to predict the course of dementias based on a nerve region's connectivity to a disease hot spot.
A study published in PLOS ONE found that Toxoplasma gondii infection suppressed the immune system, leading to a significant decrease in b-amyloid plaque deposition and improved performance in behavior tests like the water maze. This suggests that the parasite may have favorable effects on Alzheimer's disease progression.
Research published in JCI suggests a connection between insulin resistance and Alzheimer's disease, highlighting potential new therapeutics for treatment. The studies found that defective insulin signaling is a common feature of Alzheimer's disease and that treatment with a new anti-diabetic drug normalized insulin signaling and improv...
Research suggests a connection between insulin resistance and Alzheimer's disease, with defective insulin signaling potentially impacting cognitive function. Studies show that treating Alzheimer's disease with anti-diabetic drugs can normalize insulin signaling and improve cognitive function.
The university will lead the clinical trials, which aim to determine if Alzheimer's disease can be halted or delayed before symptoms appear. Researchers plan to give promising pharmaceuticals to family members with early-onset Alzheimer's gene and biological markers of disease.
A clinical trial examining the antioxidant effects of a vitamin E and C combination on Alzheimer's disease found no association with changes in cerebrospinal fluid biomarkers. However, the treatment was shown to reduce oxidative stress in the brain, but at the cost of faster cognitive decline.
Researchers at the University of Rochester Medical Center have developed a compound that targets RAGE, a molecular actor involved in Alzheimer's disease. The compound, FPS-ZM1, reverses amyloid deposits, restores brain blood flow, and improves learning capabilities in mice.
A cancer compound called epothilone D has been found to slow neurological damage and improve memory in a mouse model of Alzheimer's disease. The treatment prevented tau tangle formation and improved learning and memory tests, suggesting potential therapeutic benefits.
A study published in the Journal of Neuroscience shows that EpoD prevents further neurological damage and improves cognitive performance in a mouse model of Alzheimer's disease. The drug acts by stabilizing microtubules, potentially improving nerve-cell function in AD and other diseases.
Researchers at McGill University have discovered a critical process in understanding the degeneration of brain cells sensitive to Alzheimer's disease. The study suggests that targeting this process could lead to alternative therapies for treating AD, including drugs that protect neurons from degeneration.
Researchers validated protease cathepsin B as a target to improve memory deficits and reduce amyloid plaque pathology in an animal model representative of most AD patients. Deleting the CatB gene improved memory deficits while reducing amyloid plaque, mimicking that found in AD.
A new study suggests that extending treatment to moderate to severe Alzheimer's disease patients with the commonly used dementia drug donepezil can help treat more patients worldwide. The trial found that continued treatment resulted in improved cognitive and functional abilities, with benefits noticeable to patients for at least a year.
Researchers at University College London have discovered specific antibodies that block the toxic effect of Amyloid-ß on synapses, raising hopes for a treatment to combat early cognitive decline. The findings suggest targeting the secreted protein Dkk1 could offer an effective treatment to protect synapses.
Researchers discovered that vitamin D3 activates key genes and cellular signaling networks to stimulate the immune system to clear amyloid-beta protein from the brain. The study provides new insights into the potential therapeutic benefits of vitamin D3 for Alzheimer's disease treatment.
Researchers found that higher levels of VILIP-1 in the spinal fluid are linked to faster mental decline in patients with early Alzheimer's disease. This study suggests that VILIP-1 may be a better predictor of Alzheimer's progression than other markers.
A scientific method paper and video demonstrating a laboratory technique used to study mitochondrial dysfunctions in Alzheimer's disease and other disorders has gone viral. The technique, which measures the electrical potential across the inner mitochondrial membrane, has been accessed by more than 14,000 scientists worldwide.
Researchers at MGH found that isoflurane impairs learning and memory in mice by damaging mitochondria, while desflurane has no similar effects. The study suggests desflurane may be a better anesthetic for patients with Alzheimer's disease.
Researchers at Stanford University highlight potential treatments for cognitive dysfunction in Down syndrome, which shares similarities with Alzheimer's disease. The review focuses on insights from animal models and structural abnormalities in the DS brain.
Researchers found that mitochondrial dysfunction occurs early in Alzheimer's disease, before symptoms like memory loss appear. The study discovered altered mitochondrial movement, structure, and energy dynamics in the brain of genetically modified mice with familial Alzheimer's disease.
Scientists have discovered that inhibiting the HDAC2 enzyme can reverse Alzheimer's symptoms in mice by removing gene 'blockades' that shut off memory formation. This finding suggests that targeted drugs could be effective in treating the disease, which affects millions worldwide.
Researchers have found that an epigenetic blockade affects people with Alzheimer's disease, leading to a blockade of genes involved in learning and memory. A treatment approach using gene therapy reduced HDAC2 levels, preventing the blockade and improving neuroplasticity.
Scientists at Simon Fraser University have discovered a new approach to treating Alzheimer's disease by targeting a specific enzyme. By maintaining the correct balance of sugars in brain proteins, they hope to slow or prevent the development of the fatal condition.
A University of Miami study reveals alarming accumulation of BMAA in shark fins, which may pose a significant threat to shark fin consumers. The study found levels of BMAA ranging from 144 to 1836 ng/mg, similar to those measured in the brains of Alzheimer's and ALS victims.
Researchers at Cedars-Sinai are exploring new treatments for Alzheimer's disease by targeting the immune system and amyloid plaques in the brain. The goal is to identify drugs that can stimulate macrophages to clean up these plaques, allowing brain regeneration.
Research suggests that disrupted sleep patterns may be associated with the build-up of amyloid plaques in the brains of people without memory problems. The study found that participants who woke up more than five times per hour and slept inefficiently were more likely to have these markers.
Researchers found that curcumin prolongs the lives of fruit flies with Alzheimer's symptoms by up to 75% and maintains their mobility. However, it did not dissolve or decrease the amyloid plaque, but instead accelerated its formation by reducing precursor forms.
A UCLA-developed brain-imaging tool detects abnormal protein deposits associated with Alzheimer's disease and tracks progression over time. The technique, using FDDNP-PET scans, predicts cognitive decline in individuals with mild cognitive impairment and normal aging, offering potential early detection and treatment of Alzheimer's.
A study published by the American Academy of Neurology suggests that consuming excessive calories may double the risk of mild cognitive impairment (MCI) in individuals aged 70 and above. The findings indicate a dose-response pattern where higher caloric intake corresponds to increased MCI risk.
Researchers discover bexarotene rapidly clears amyloid from the brain and reverses cognitive deficits in mouse models of Alzheimer's disease. The results show significant promise for a new therapy, with more than half of amyloid plaques cleared within 72 hours.
Researchers have identified beta-arrestin, a protein that supports connections between neurons, as a crucial link to short-term memory. By regulating synaptic plasticity, beta-arrestin plays a key role in the formation and disassembly of neural connections, which can help prevent Alzheimer's disease.
A large study found that mild cognitive impairment is consistently associated with higher disability and neuropsychiatric symptoms, particularly anxiety, apathy, and irritability. The prevalence of mild cognitive impairment ranged from 0.8% to 4.3% in eight low- and middle-income countries.
According to a study published in Archives of Neurology, revised criteria for mild cognitive impairment (MCI) may reclassify patients with very mild or mild Alzheimer's disease dementia. The new guidelines allow for more flexibility in defining functional independence, potentially affecting diagnostic approaches and treatment options.
New research reveals that tau oligomers, smaller structures formed before neurofibrillary tangles, are the most toxic entities in Alzheimer's. High levels of tau oligomers have been found in some Alzheimer's brains, and their presence has been linked to various biochemical behaviors and structures.
A new questionnaire, AQ, can discriminate between normal memory loss and aMCI, a precursor to Alzheimer's disease. The study found that four questions were strong indicators of aMCI, including repetition of questions and difficulties with finances and direction.
A new study published in PloS One suggests that abnormal tau protein propagates along linked brain circuits, jumping from neuron to neuron. This finding opens new opportunities for studying Alzheimer's disease and developing therapies to halt its progression.
A study published in Neurology found that high levels of beta-amyloid in the brain are associated with subtle changes in memory and mental function in healthy adults. The study, which involved 137 participants aged 30-89, also linked higher amounts of beta-amyloid to lower test scores in working memory, reasoning, and processing speed.
Researchers measured beta-amyloid levels in healthy adults between 30 and 90 years old, finding that high levels correlated with cognitive deficits. The study suggests subtle effects on cognition occur early, highlighting the need for interventions to slow or halt disease progression.
The study found rare variants in key Alzheimer's-related genes in 13% of analyzed samples, with 5% likely contributing to the disease. The findings suggest a common disease mechanism for both early- and late-onset Alzheimer's, leading to potential changes in classification.
Scientists at UC San Diego School of Medicine have created in vitro models of sporadic and hereditary Alzheimer's disease using induced pluripotent stem cells. The living cells provide an unprecedented tool for developing and testing drugs to treat the disorder, offering a new method for understanding the cause of the disease.
Researchers at Temple University have discovered a protein that regulates amyloid beta production and controls a biochemical chain reaction linked to Alzheimer's development. The protein, 12/15-Lipoxygenase, targets Beta secretase (BACE-1), an enzyme key to amyloid plaque formation.
Researchers have developed a non-invasive method to diagnose Alzheimer's disease using infrared analysis of white blood cells. The technique distinguishes between mild and moderate stages of the disease, allowing for reliable early diagnosis.
A new study reveals that people with no symptoms of Alzheimer's who engaged in cognitively stimulating activities throughout their lives had fewer deposits of beta-amyloid, a destructive protein that is the hallmark of the disease. Lifelong cognitive engagement may affect a primary pathological process in the disease, suggesting potent...
Researchers found a direct association between cognitive engagement and lower levels of β-amyloid protein, which is associated with Alzheimer's disease. Participants who engaged in cognitively stimulating activities had reduced β-amyloid uptake, while those with the lowest activity had higher uptake comparable to patients with AD.
Researchers identified a series of synthetic compounds that interfere with the self-assembly of amyloid beta peptides, satisfying an initial condition for Alzheimer's treatment. Disordered peptide structure controls interactions with active compounds.
Scientists have developed an imaging agent that binds to signs of Alzheimer's disease, including ß-amyloid plaques and neurofibrillary tangles. The agent, called FPPDB, has shown promise for early diagnosis in laboratory tests.
A recent study published in the Western Journal of Nursing Research found that exposure to blue-green light has therapeutic effects on Alzheimer's disease patients. Patients treated with this type of light showed improved recognition, recollection, and motor coordination, as well as enhanced moods and personalities.
A new study published in The Lancet shows that memantine is ineffective for patients with Alzheimer's disease and Down syndrome aged 40 years and older. The drug was tested on 88 patients with or without dementia, but showed no significant improvement in cognition and function compared to a placebo group.
A study at UCLA has identified 56 proteins that show significant differences between people with familial Alzheimer's disease and those without it. The changes may represent an early manifestation of the loss of critical brain structures, providing potential new targets for drug interventions.
A clinical trial found that using a nicotine patch for six months improved long-term memory in people with mild cognitive impairment by 46%. The study, published in Neurology, suggests that nicotine may be beneficial for early signs of memory loss.
Sathyanaryanan Puthanveettil, a Scripps Research scientist, has been awarded two notable grants to study the critical component of long-term memory formation. He will investigate the role of kinesin in this process using the marine snail Aplysia.
Researchers have identified a 90% accuracy biomarker that increases the risk of developing Alzheimer's by 10 years. Patients with low levels of beta-amyloid and high tau protein levels are at highest risk, indicating potential therapeutic targets for early intervention.