Articles tagged with Alzheimer Disease
Researchers at Hebrew University created a molecule that reduces brain cell death in diabetic rats by lowering inflammatory processes. This finding represents the first evidence of high blood sugar's link to an inflammatory pathway in the brain.
Researchers found significantly higher levels of DDE, a long-lasting metabolite of DDT, in Alzheimer's patients compared to healthy controls. Elevated DDE levels increased the risk of Alzheimer's by a factor of four.
A Rutgers University study links pesticide exposure to increased Alzheimer's disease risk, particularly in those over 60. Higher levels of the DDT compound were found in late-onset Alzheimer's patients' blood compared to controls.
A new study found that an early onset of dietary treatment may slow down the progression of Alzheimer's disease. The research, conducted on mice, suggests that even slight changes in diet composition can lead to significant changes in brain metabolism and improved memory performance.
Researchers identified a critical regulator of BACE1, an enzyme involved in Alzheimer's disease pathology. The study found that levels of this regulating protein, Rheb, are decreased in the brains of Alzheimer's patients and may be a significant factor in disease progression.
Scientists have discovered a simple single-celled amoeba that can help understand the function of human proteins in causing Alzheimer's disease. This discovery allows for animal-free testing, paving the way for potential improved treatments for the degenerative disease.
A recent Alzheimer's trial failed to produce cognitive improvement for volunteers, but researchers have identified key takeaways to inform the development of new treatments. Lessons learned include testing drugs in individuals building up amyloid plaques, giving higher doses safely, and combining disease-modifying treatments.
A recent study published in Neurology suggests that fish oil consumption may help preserve brain cells by increasing total brain volume and hippocampus area size. The study found that higher levels of omega-3 fatty acids were associated with larger brain volumes, equivalent to a delay of one to two years of brain health.
A contest for the best particle tracking technique found that each method has its own strengths, but none were deemed unequivocally superior. The challenge, which aimed to track hundreds of intracellular organelles, was marked by oversimplification in image series, limiting algorithm performance on real data.
Scientists have identified an epigenetic lesion in the hippocampus of Alzheimer's patients, which regulates tau protein and may contribute to disease progression. This discovery provides a potential new target for future therapies, offering hope for improved treatment options.
Researchers at Cleveland Clinic have identified a critical role for the Neuroligin-1 protein in Alzheimer's-related memory loss, disrupting synaptic networks and leading to memory decline. The discovery may provide new approaches for preventing and treating Alzheimer's disease.
A new study found that the presence of a gene variant APOE epsilon 4 is associated with accelerated brain atrophy rates in individuals with mild cognitive impairment. The study used MRI to measure brain atrophy over a 12- to 48-month period and found that epsilon 4 carriers exhibited greater atrophy rates than non-carriers.
Scientists at Rensselaer Polytechnic Institute discovered the structural effects of V44M and V44A genetic mutations linked to FAD. The mutations lead to increased production of toxic Amyloid Beta 42 peptide, driving memory failure in patients.
Scientists have identified fourteen genes that may be implicated in Alzheimer's disease and one gene that shows inflammation plays a crucial role in the brain of Alzheimer's patients. The study provides new insight into the cause of the disease, offering potential targets for drug discovery.
Researchers at NYSCF and Columbia University Medical Center successfully generated iPS cells from frozen brain tissue, allowing for the study of Alzheimer's disease at a cellular level. The new stem cell lines will enable drug testing on cells from patients with confirmed diagnoses.
Vitamin E, a fat-soluble antioxidant, has been shown to slow functional decline and reduce caregiver time in patients with mild to moderate Alzheimer disease. In contrast to previous trials, this study found no significant increase in mortality risk with vitamin E, suggesting potential cost-effectiveness.
A new study found that vitamin E delays progression of functional decline by 19% per year, translating into a 6.2-month benefit over placebo. Vitamin E is also easy to purchase and inexpensive, making it a potential treatment strategy for mild-to-moderate Alzheimer's disease.
Research from UC Davis Health found that high HDL and low LDL cholesterol levels are associated with lower brain amyloid plaque deposits, a hallmark of Alzheimer's disease. This study provides evidence for the importance of cholesterol management in preventing cognitive decline.
A new study suggests that a history of concussion may be related to the buildup of Alzheimer's-associated plaques in the brain. In people with memory and thinking problems, higher levels of amyloid plaques were found compared to those without head trauma.
Researchers have developed a technique combining cell transplantation and gene therapy to target BACE1, the key enzyme in amyloid beta protein production. This approach reduces Aβ protein production by downregulating the BACE1 gene, offering new therapeutic avenues for Alzheimer's disease.
Researchers used high-resolution fMRI to identify where Alzheimer's disease starts, spreads from the lateral entorhinal cortex (LEC) to other areas of the cerebral cortex. LEC dysfunction occurs when changes in tau and amyloid precursor protein (APP) co-exist, damaging neurons that then spread to adjoining regions.
Scientists use reactive glial cells to regenerate healthy neurons in a breakthrough technology for treating brain injuries and Alzheimer's disease. In mouse models and human cell cultures, the method successfully converts glial cells into functional neurons.
A study published in Neuron found that the posterior cingulate cortex (PCC) is active when the brain isn't working hard and quiets down during peak performance. The PCC plays a crucial role in monitoring performance and improving it, particularly in challenging cognitive tasks.
A team of researchers has identified a critical balance point between tau and a master cellular regulator disrupted by amyloid-beta oligomers, driving adult neurons into cell cycle re-entry and eventual death. The study suggests that the protein complexes mTORC1 and mTORC2 play a key role in regulating this process.
A research team has discovered a second rare genetic mutation that strongly increases the risk of Alzheimer's disease in later life. The mutation is found in the Phospholipase D3 (PLD3) gene, which influences amyloid precursor protein processing and may be a potential therapeutic target.
A study in mice reveals that breakdown of brain blood vessels may amplify problems associated with Alzheimer's disease. Pericytes, a type of blood vessel cell, may provide novel targets for treatments and diagnoses.
Researchers found elevated BACE1 activity in mild cognitive impairment patients, suggesting it may be an early indicator of Alzheimer's disease. Increased BACE1 enzymatic activity correlated with plaque numbers and cognition status.
Researchers have identified two rare gene variants in the phospholipase-D 3 gene (PLD3) that double an individual's risk of developing late-onset Alzheimer's disease. The study found that these variants were present in affected family members but not in healthy elderly relatives, suggesting a significant role in disease development.
A large EU study is investigating whether nilvadipine can help patients with Alzheimer's disease by reducing the formation of amyloid plaques in animal brains. The clinical trial will involve 500 patients in nine European countries, who will be treated with nilvadipine or a placebo for eighteen months.
Researchers at UC Irvine's Institute for Memory Impairments and Neurological Disorders have received a grant to develop and study patient-derived stem cell lines. The UCI MIND team will create up to 40 sets of induced pluripotent stem cells to explore the biology of Alzheimer's disease and test novel therapeutic approaches.
Robert Mahley and his team will use the funding to identify new chemical compounds that can target apolipoprotein E4 (apoE4), the strongest genetic risk factor for developing Alzheimer's. They aim to develop small-molecule therapies that prevent apoE4's damaging effects on the brain.
Researchers at OHSU discovered a way to use small molecules to fix misfolded proteins, allowing them to function normally again. This technique has the potential to treat diseases such as cystic fibrosis, cataracts, and Alzheimer's disease.
Scientists transform skin cells into nerve cells from patients with Alzheimer's disease and test several non-steroidal anti-inflammatory drugs. The results show that these compounds have no effect on the harmful beta-amyloid aggregates in human neurons, unlike in animal models.
Researchers at University of Pennsylvania develop method to deliver protein across blood-brain barrier, degrading Alzheimer's plaques by up to 70% in mice brains and human brain tissue. The approach uses cholera toxin B as carrier and myelin basic protein to break down amyloid beta chains.
Researchers found that pre-moxibustion prior to Aβ1–42 exposure was more effective than moxibustion after Aβ1–42 exposure in protecting neuronal structure and lowering apoptosis rate. Moxibustion therapy may have a beneficial effect on preventing Alzheimer's disease development.
A study by Dr. Sha Liu and colleagues found that progesterone administration can reverse cognitive impairment in Alzheimer's disease patients. The research, published in Neural Regeneration Research, used rat models to demonstrate the protective effect of progesterone against Aβ25–35-induced neurotoxicity.
Researchers used induced pluripotent stem cells to test NSAIDs on human neurons, finding they failed to respond despite initial success in cell and animal models. The study highlights the importance of testing compounds directly in authentic human cells for more reliable drug development approaches.
St. Jude Children's Research Hospital scientists have identified an enzyme that can halt or reverse the build-up of toxic protein fragments in mice with Alzheimer's disease. Gene therapy increased activity of the enzyme neuraminidase 1, reducing plaques in the brain involved in learning and memory.
A new study from CAMH found that people carrying the SORL1 gene for Alzheimer's disease show brain changes beginning in childhood. These changes are linked to an increased risk of late-onset Alzheimer's, a condition that typically appears decades later.
Selim Zilkha has pledged $5 million to the University of Southern California - Health Sciences to support a new endowed chair in Alzheimer's disease research. This gift brings his total commitment to neuroscience research at the Keck School to over $30 million.
Researchers at the Hebrew University of Jerusalem discovered a new compound, NT219, that selectively inhibits the aging process to protect the brain from neurodegenerative diseases. The compound's inhibition of IGF1 signaling pathway has therapeutic potential for treating neurodegenerative disorders like Alzheimer's and Parkinson's.
A study analyzing resting-state functional MRI data from four populations reveals that Alzheimer's disease is associated with a decline in brain network efficiency. As cognitive deficits increase, the shortest path in the network increases while clustering coefficients decrease.
Researchers found brain growth differences in infants carrying APOE-E4 gene, which increases risk for late-onset Alzheimer's. The study suggests early changes may provide a 'foothold' for disease pathologies.
Researchers found that disabling a circadian clock gene blocks the brain's antioxidant surge, allowing free radicals to cause more damage. This can lead to neurodegeneration and age-related brain cell injury, similar to Alzheimer's disease.
Researchers found that introducing protective variant APOE2 into brains of animals with established plaques reduced amyloid beta deposition, retention and neurotoxicity. This suggests the potential for gene-therapy-based treatment to alleviate Alzheimer's disease progression.
A pilot study found that meditation and mindfulness-based stress reduction improved functional connectivity in the brain, reducing hippocampal atrophy associated with Alzheimer's disease. Researchers suggest this intervention may contribute to improved quality of life for patients with cognitive decline.
Researchers used genetic engineering to precisely study a key protein's role in familial Alzheimer's disease, discovering that simple loss-of-function doesn't contribute to the inherited form. The findings could help elucidate Alzheimer's mechanisms and inform drug development.
Researchers found that people with higher pulse pressure in middle age are more likely to have Alzheimer's biomarkers in their spinal fluid. For every 10 point rise in pulse pressure, the average level of p-tau protein rose by 1.5 picograms per milliliter.
Researchers found significant loss of neurons in the retina's inner nuclear and ganglion cell layers, suggesting Alzheimer's disease presence. The study suggests a potential new way to diagnose or predict Alzheimer's through eye examination, using optical coherence tomography.
A new compound has been found to inhibit cognitive impairment in animal models of Alzheimer's disease, showing a 60% improvement in learning and memory. The research uses the Endothelin system to target potential treatments for AD.
Researchers are exploring the role of innate immunity in Alzheimer's disease, hoping to identify novel therapies. By analyzing gene expression and RNA transcripts, they aim to understand the immune response's impact on the disease.
Researchers developed a statistical model that can identify individuals with mild cognitive impairment who are at risk of developing dementia, enabling earlier diagnosis and treatment. The model takes into account various factors such as age, sex, race, and education to provide a more accurate prognosis.
A study found increased deposits of β-Amyloid (Aβ) plaques in some areas of the brains of patients with traumatic brain injury (TBI). Researchers discovered Aβ plaque increases may be linked to TBI and accelerated Alzheimer's Disease progression.
A new method predicts the time from Alzheimer's disease onset to full-time care, nursing home residence, or death with high specificity. The method uses a complex model based on data gathered from a single patient visit and can predict outcomes such as time to assisted living or incontinence.
The 'Path to 2025' Alzheimer's Disease Summit highlights the need for streamlined drug development to tackle the disease. The report estimates that current total cost of bringing an effective Alzheimer's treatment to market approaches $6 billion, nearly three times the industry average.
Research shows that speaking two languages can delay the onset of three types of dementias, including Alzheimer's disease, frontotemporal dementia, and vascular dementia. The study found that people who spoke two languages developed dementia four and a half years later than those who only spoke one language.
HS-AGING affects older adults, causing cognitive decline and memory impairment. Recent studies reveal around 20% of dementia cases are misdiagnosed as HS-Aging, highlighting the need for accurate diagnosis and exploration of new therapeutic targets to alter disease progression.
A nationwide study found that individuals with Alzheimer's are more prone to ischaemic heart diseases but undergo fewer related procedures. Despite this, reduced cognitive function was not a clear explanation for the disparity in treatment
Scientists at UCL Institute of Neurology identified a genetic mutation that leads to the production of toxic RNA molecules, potentially responsible for frontotemporal dementia and motor neuron disease. The build-up of these molecules may be key to causing the diseases.
A recent study found that S14G-humanin inhibits the toxic effects of amyloid-beta protein on hippocampal neurons, restoring cellular balance. The compound's neuroprotective effect is 1,000-fold stronger than humanin.