Articles tagged with Alzheimer Disease
Scientists at University of Maryland Biotechnology Institute discover ubiquilin controls levels of proteins central to early development of Alzheimer's disease. The molecule increases presenilin levels in cells, a key step in understanding the disease.
Researchers identified LRP-1 as a key molecule in removing beta amyloid protein from the brain through blood circulation. In healthy mice, blood vessels efficiently clear amyloid peptide, whereas impaired LRP-1 function can lead to plaque accumulation and neurodegeneration.
Scientists at Johns Hopkins have identified a specific enzyme, beta-secretase, as crucial for forming the hallmark amyloid plaques of Alzheimer's disease. The study, which used mice models, suggests that targeting this enzyme could offer new therapeutic options for treating the condition.
Researchers analyzed medical records of World War II veterans with head injuries and found a link between early adulthood trauma and later-life Alzheimer's disease. The more severe the injury, the greater the risk of developing AD, with those with severe injuries having a four-fold greater risk.
A study of caregivers' goals for Alzheimer's treatment reveals that maintaining quality of life is more important than extending lifespan. Most caregivers are willing to accept risks to slow the disease and would prioritize benefits such as preserving memory, communication, and daily function over additional years of life.
Researchers at Massachusetts General Hospital discovered a key link between presenilin gene mutations, altered calcium handling, and amyloid-beta42 production in Alzheimer's disease. Inhibiting a specific calcium pathway may lower A-beta42 levels, offering hope for preventing or slowing the progression of the devastating disease.
Studies found human evolution led to a decrease in high-risk genetic variants associated with these diseases, instead increasing protective e2 and e3 variants. Analysis suggests advantageous mutations may have driven this shift.
Researchers discovered a high incidence of Alzheimer's disease in an Arab community, suggesting a possible role for a previously unknown recessive gene. DNA analysis revealed that only 4% of participants carried the apolipoprotein E-4 gene variant, lower than expected rates in other populations.
Researchers at the University of Toronto have isolated a key protein involved in the degeneration of nerve cells in Alzheimer's disease. The newly discovered protein, nicastrin, regulates the production of amyloid beta-peptide, a toxic derivative associated with the disease.
A UC Davis study identifies brain systems affected in stroke patients with memory loss, distinguishing them from those affected by Alzheimer's disease. This distinction enables physicians to treat root causes of memory loss, such as high blood pressure or diabetes, and prevent strokes.
Researchers found that 19 out of 47 people with mild cognitive impairment who had difficulty identifying smells went on to develop Alzheimer's disease. The study suggests that the inability to recognize smells, combined with a lack of awareness about impaired olfactory senses, may be used as a predictor of impending Alzheimer's disease.
Researchers discovered a striking similarity between proteins involved in early stages of Alzheimer's disease and mad cow disease using computer modeling. The study suggests a common molecular mechanism underlying the initiation stages of these neurodegenerative diseases, potentially leading to new preventive drug targets.
Researchers at UC Irvine have discovered a protein called calsenilin that can offset calcium imbalances in brain cells, which contribute to the development of early-onset familial Alzheimer's disease. This finding may lead to pharmaceutical therapies and preventive measures to halt the progression of this neurological disorder.
Researchers found that ibuprofen significantly reduced inflammation and amyloid plaques in an animal model of Alzheimer's disease, which may help prevent the disease. The study suggests that taking anti-inflammatory drugs early on could delay the onset of AD by about a decade.
A study by Case Western Reserve University found that people with higher levels of non-occupational activities were less likely to develop Alzheimer's disease later in life. Intellectual and physical activities, such as playing musical instruments or exercising, may help ward off the disease.
Researchers use MRI and magnetic resonance spectroscopy to detect Alzheimer's disease by measuring chemical markers in the brain. The study found that this technique can distinguish patients with Alzheimer's from those without the disease and identify patterns of damage consistent with the disease.
A study of 286 patients with mild to moderate Alzheimer's disease found that treatment response to Aricept was not predicted by ApoE4 genotype or gender. Patients treated with Aricept showed significant improvements in global function and cognition, while those on placebo experienced decline.
The World Alzheimer Congress will showcase recent discoveries on Alzheimer's disease, including the link between cell suicide and amyloid protein accumulation. Researchers also explored the role of apoE4 in driving brain damage and cognitive decline.
A study by Dr. David Bennett found that many people with mild cognitive impairment exhibit Alzheimer's disease pathology, indicating a larger public health problem than previously thought. The research suggests increased funding for clinical care and research is needed to combat the disease effectively.
Patients with dementia often receive inadequate medical care due to a lack of data on the safety and efficacy of treatments. Guidelines need to consider a patient's ability to comprehend, remember, and follow directions, as well as their caregiver's capacity to listen and act.
The American Academy of Neurology has issued guidelines to help determine whether people with Alzheimer's disease should continue driving. Drivers with Alzheimer's have a substantially increased rate of accidents and driving performance errors, posing a significant traffic safety risk.
Two new Phase III studies published in Neurology show that Reminyl (galantamine) significantly improves cognition, global function, and behavioral symptoms of Alzheimer's disease over a period of 12 months. The treatment also maintains activities of daily functioning for patients with mild to moderate Alzheimer's disease.
Researchers at the University of Pennsylvania School of Medicine have created a stealth-like molecule called BSB that can effectively breach the blood-brain barrier and bind to amyloid plaques, enabling visualization using PET or SPECT imaging. This breakthrough paves the way for the refinement of BSB as a diagnostic tool for Alzheimer...
A study published in Neurology found that estrogen had no effect on improving memory and mental functions in postmenopausal women with mild to moderate Alzheimer's disease after a 12-week period. Researchers suggest further trials are needed to determine the effectiveness of estrogen in preventing or delaying the onset of Alzheimer's.
Researchers found that telomerase blocks a biochemical cascade of reactions called apoptosis, which causes nerve cell self-destruction. High levels of telomerase display remarkable resistance to damage or death in experimental models of Alzheimer's disease or stroke.
A study found that the plasmin system, which regulates blood clots, may also play a role in Alzheimer's disease. The researchers suggest that destroying amyloid-beta protein deposits with tPA could be a potential treatment for the disease. Further research is needed to confirm this model and explore its effectiveness.
Researchers at the University of Kentucky have discovered a new potential target for compounds that may treat or prevent Alzheimer's disease. The receptor RAGE interacts with amyloid fibrils, accelerating fibril formation and inducing cellular dysfunction.
Researchers at UT Southwestern Medical Center have developed an easy and inexpensive index to measure the severity of Alzheimer's disease. The index correlates a simple lab test determining platelet Alzheimer's plaque protein (APP) in blood with cognitive decline, as measured by the Mini-Mental State Exam.
A team of scientists led by Li-Huei Tsai found that the enzyme calpain triggers neurodegeneration in brain cells, similar to Alzheimer's disease. The discovery proposes a common mechanistic link between toxic insults and brain cell injury, offering potential targets for drugs to slow or stop progression.
Researchers found that a synthetic protein resembling the herpes simplex virus mimics beta-amyloid, a toxic agent in Alzheimer's patients. This connection could lead to the development of vaccines or drugs to prevent or treat Alzheimer's disease.
A new imaging technique reveals disrupted microcolumns in brains affected by Alzheimer's disease and Lewy body dementia, suggesting a link between microcolumn organization and cognitive impairment. The study found that the absence of microcolumns correlates with the number of fibrillary tangles, but not senile neuritic plaques.
Research suggests that occupational lead exposure significantly increases the risk of developing Alzheimer's disease, particularly among those working in jobs with high levels of lead exposure. The study found a strong correlation between lead exposure and Alzheimer's, while other metals such as aluminum and solvents were not associate...
A study by the American Academy of Neurology found that people with higher levels of non-occupational activities, such as playing a musical instrument or gardening, were less likely to develop Alzheimer's disease later in life. Researchers also discovered that it is never too late to get started with intellectual activities.
A new study suggests Reminyl, a treatment for Alzheimer's disease, provides significant cognitive and functional improvements in patients. The medication has been shown to delay the emergence of behavioral symptoms and maintain daily functioning for up to a year.
A new study by the Gladstone Institute of Neurological Disease and UCSF team found that apoE3 can inhibit memory problems associated with Alzheimer's disease, while apoE4 cannot. This discovery could lead to the development of new drugs simulating apoE3's protective quality.
Researchers found that apoE4, a high-risk version of the lipoprotein, directly promotes the development of neuritic plaques in the brain by enabling amyloid-beta to form into hair-shaped fibrils. ApoE3 had less damaging effects. The study used a mouse model and showed that apoE interaction with amyloid-beta leads to neurodegeneration.
Researchers at Weizmann Institute have discovered the 3-D interaction between galanthamine and brain enzyme acetylcholinesterase (AChE), which breaks down neurotransmitter acetylcholine in Alzheimer's disease. This finding may lead to a new family of drugs with reduced side effects.
A study found that people with Alzheimer's disease were 50% more likely to have depression symptoms than those without the disease. Depression symptoms such as lack of interest and loss of energy were three times more common in those who later developed Alzheimer's.
Harvard Medical School scientists identify protein p25 as a possible trigger for Alzheimer's disease by turning brain enzyme cdk5 into a menace. The study supports one of two major hypotheses explaining the complex condition, offering a new handle on underlying molecular pathways.
Researchers identified a molecule that triggers the formation of deadly protein snarls in Alzheimer's disease. High levels of a shortened, malfunctioning version of the protein p35 in brains lead to hyperphosphorylation of tau protein, causing neurofibrillary tangles.
A new transgenic mouse model develops damaging tau protein tangles as it ages, exhibiting clinical symptoms similar to tauopathies. The tau mouse is expected to aid in understanding the role of tau tangles in Alzheimer's disease and other neurodegenerative diseases.
Scientists have created a genetically-engineered mouse model with human tau genes, allowing for the study of tau-containing lesions in various brain disorders. The new model shows abnormal tau filaments accumulating in nerve cells, similar to those found in Alzheimer's disease.
Paul Coleman, a renowned neuroscientist, has been awarded $1 million by the Alzheimer's Association to investigate the earliest signs of Alzheimer's disease. His research team aims to develop a simple test that can detect the disease in its initial stages, potentially allowing for earlier diagnosis and treatment.
A recent Mayo Clinic study found that traumatic brain injuries increase the risk of Alzheimer's Disease, with a median observed time from injury to onset of 10 years. The study suggests that traumatic brain injury interacts with other factors to hasten the onset of Alzheimer's in susceptible individuals.
Researchers from Mount Sinai Hospital and University of Toronto have discovered that Alzheimer's disease proteins also play a crucial role in mammalian development. The study used mice lacking PS1 and PS2 genes to investigate their normal function, finding that these proteins are essential for brain development.
Researchers identify Notch signaling pathway involved in switching from brain cell growth to stability, which could lead to new treatments for neurological disorders. The study provides a clue on how the transition from growth to stability occurs in the brain.
Researchers have identified a new molecular marker for Alzheimer's disease, a normal cellular enzyme called casein kinase-1 (CK-1), which accumulates in nerve cells damaged by AD. CK-1 levels were found to be abnormally high in vacuoles within the hippocampus region of AD brains.
The Oregon Center for Complementary and Alternative Medicine in Neurological Disorders (ORCCAMIND) has been established at OHSU with a $7.8 million NIH grant. Initial research projects focus on herbal medicines, yoga, and other alternative therapies for Alzheimer's disease and multiple sclerosis.
Researchers found that brain trauma causes microscopic damage in the brain, leading to the formation of Alzheimer's-like plaques. The study supports previous evidence linking brain trauma to increased risk of developing Alzheimer's disease later in life.
A new imaging method is being developed to show images of plaque deposits in the brains of Alzheimer's patients as the disease progresses. The technology uses technetium-based probes to detect amyloid plaque deposits, which could allow for definitive diagnosis before death.
Researchers created genetically engineered mice with pathological characteristics of Alzheimer's disease, providing a new model for studying the disease. The mice exhibit amyloid deposits similar to those found in human patients, and further elevation of beta-amyloid accelerates the age of onset of pathological changes.
Researchers identified Pin1, an enzyme that may restore tau protein function, and found it depleted in Alzheimer's brains. This could lead to new treatments for the disease by preventing tau protein misfolding.
A novel gene, BRI, located on chromosome 13 has been identified as responsible for familial British dementia, a rare inherited disease that causes progressive dementia and spasticity. The discovery provides new clues to the abnormal changes in the brain that lead to dementia.
A team of scientists has found a critical interaction between two brain proteins that could help explain the death of nerve cells in Alzheimer's disease. The discovery reveals that normal APP provides a protective function against cell death, while mutant forms do not.
Researchers found a new mechanism explaining how Alzheimer's disease damages the brain by producing hydrogen peroxide from oxygen, a toxic agent that can cause brain damage. The discovery provides a potential target for new drugs to treat Alzheimer's, which affects four million Americans.
New research from Washington University in St. Louis suggests that false recall in older adults with Alzheimer's is related to attention breakdowns rather than memory decline. The study found that older adults are susceptible to creating false memories, which challenges the idea of a broad general decline in all memory-related functions.
A recent study by Brown University researchers has found a link between agrin protein and Alzheimer's disease plaques. The protein, involved in nervous system development, may play a role in the disease's progression.
Researchers have developed new chemicals that target the butyrylcholinesterase enzyme, which may help attack Alzheimer's disease. The study's findings suggest that inappropriate BChE activity increases the risk and progression of Alzheimer's disease, and preliminary studies indicate improved cognition and learning in rodents.
A team of researchers has determined that a gene on chromosome 12, previously suspected to be a strong genetic risk factor for Alzheimer's disease, cannot be replicated. Despite the initial findings, there is strong evidence for another genetic defect elsewhere on the chromosome that causes Alzheimer's disease.
Researchers discovered that a mutant form of the presenilin-1 protein causes a significant reduction in amyloid formation. The study provides insight into the interaction between two key molecules involved in amyloid formation, which may lead to advances in therapeutics research.