Read the latest research on Alzheimer's disease. Learn about Alzheimer's symptoms such as memory loss and senile dementia. Find out about Alzheimer's stages, causes and new treatments.
Updated: 27 min 58 sec ago
A new therapy prompts immune defense cells to swallow misshapen proteins, amyloid beta plaques and tau tangles, whose buildup is known to kill nearby brain cells as part of Alzheimer's disease, a new study shows.
Links between lipid imbalance and disease have been established, in which lipid changes increase the formation of amyloid plaques, a hallmark of Alzheimer's disease. This imbalance inspired researchers to explore the role of lipids comprising the cellular membranes of brain cells. In Biointerphases, the researchers report on the significant role lipids may play in regulating C99, a protein within the amyloid pathway, and disease progression.
A new study not only sheds light on how the APOE4 gene may cause some of the pathologies associated with Alzheimer's disease, but also suggests a new treatment target that might help people who carry the APOE4 gene in early and late stages of the disease. Researchers found that APOE4 is associated with the activation of an inflammatory protein that causes a breakdown in the blood-brain barrier which protects the brain.
Scientists explore how protein and signaling pathways change in patients with Alzheimer's disease. Their work creates a new model of disease progression, taking advantage of the heterogeneity that is inherent to human studies.
A new imaging technique has the potential to detect neurological disorders -- such as Alzheimer's disease -- at their earliest stages, enabling physicians to diagnose and treat patients more quickly. Termed super-resolution, the imaging methodology combines position emission tomography (PET) with an external motion tracking device to create highly detailed images of the brain.
A new study has identified mechanisms by which COVID-19 can lead to Alzheimer's disease-like dementia. The findings indicate an overlap between COVID-19 and brain changes common in Alzheimer's, and may help inform risk management and therapeutic strategies for COVID-19-associated cognitive impairment.
Researchers have identified a previously unknown early driver of Alzheimer's disease (AD) and vascular dementia (VaD). They report high levels of cis P-tau, a pathogenic protein, in human AD and VaD brains as well as preclinical disease models. Treatment with an antibody to the toxic protein prevented disease progression and reversed disease symptoms and restored cognitive function in older mice.
Much like a supply truck crossing the countryside, the misfolded proteins that damage neurons in Alzheimer's disease travel the 'roads' of the brain, sometimes stopping and sometimes re-routing to avoid roadblocks.
Until now, systemic biomarkers to measure exercise effects on brain function and that link to relevant metabolic responses were lacking. A study shows a memory biomarker, myokine Cathepsin B (CTSB), increased in older adults following a 26-week structured aerobic exercise training. The positive association between CTSB and cognition, and the substantial modulation of lipid metabolites implicated in dementia, support the beneficial effects of exercise training on brain function and brain health in asymptomatic individuals at risk for Alzheimer's.
The team looked in different regions of the brain, which are affected in Alzheimer's disease before looking for common changes across these cortical regions. They identified 220 sites in the genome, including 84 new genes, which showed different levels of DNA methylation in the cortex in individuals with more severe Alzheimer's disease, which weren't seen in the cerebellum.
A study of nearly 2,500 adults found that having trouble falling asleep, as compared to other patterns of insomnia, was the main insomnia symptom that predicted cognitive impairment 14 years later.
Researchers now report a high-throughput target and drug discovery platform using motor neurons made from ALS patients. Using the platform, they confirmed two known targets and identified an existing class of drugs -- agonists to the dopamine D2 receptor -- as potential novel treatments.
Weakened electrical signals in the brain may be an early warning sign of age-related neurodegenerative diseases such as Alzheimer's disease.
Scientists have observed for the first time what it looks like in the key memory region of the brain when a mistake is made during a memory trial. The findings have implications for Alzheimer's disease research and advancements in memory storage and enhancement, with a discovery that also provides a view into differences between the physiological events in the brain during a correct memory versus a faulty one.
An international study has identified a new drug to stop athletes developing dementia after sustaining repeated head injuries in their career.
A new study has identified a molecule called ten-eleven-translocation 1 (TET1) as a necessary component in the repair of myelin, which protects nerves and facilitates accurate transmission of electrical signals. The discovery could have important implications in treating neurodegenerative diseases and for molecular rejuvenation of aging brains in healthy individuals.
A new study of over 3000 people, has shown for the first time that a single biomarker can accurately indicate the presence of underlying neurodegeneration in people with cognitive issues.
Researchers have discovered that the immune cells that protect the brain and spinal cord come primarily from the skull. The finding opens up the possibility of developing therapies to target such cells as a way to prevent or treat brain conditions.
New research into Alzheimer's disease (AD) suggests that secondary infections and new inflammatory events amplify the brain's immune response and affect memory in mice and in humans -- even when these secondary events occur outside the brain.
Recent failed clinical trials of a drug designed to clear the mutant Huntingtin protein that causes Huntington's disease (HD) heightens the need for new approaches for the devastating, incurable, progressive neurodegenerative genetic disorder. Scientists have found that the targeting the protein called FK506-binding protein 51 or FKBP51 promotes the clearing of those toxic proteins via autophagy, a natural process whereby cells recycle damaged proteins and mitochondria and use them for nutrition.