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Exposure to traffic-related air pollution is linked to higher levels of amyloid plaques in the brain, according to a postmortem study. The study examined the brain tissue of 224 individuals in Atlanta who agreed to donate their brains after death. The researchers also analyzed the amount of fine particulate matter from traffic-related air pollution at participants' home addresses in the years leading up to their death. The study found that higher exposure to air pollution in the year before death was associated with a nearly twofold increase in the likelihood of higher levels of plaques, while higher exposure in the three years before death was associated with an 87% higher likelihood. The study suggests that further research is needed to establish a causal relationship between air pollution and Alzheimer's disease. [Extracted from the article]

This article, titled "Snagged," features two poems by Tamara Baer and Greg Berg. Baer's poem describes a moment of disorientation and wonder when encountering a potted palm in a shopping mall. The poet reflects on the sensation of touching the plant and compares it to the feeling of diving underwater and resurfacing for air. Berg's poem explores the theme of love and memory, depicting a person with dementia and their fading ability to communicate. Both poets have previous publications and are based in Santa Fe. [Extracted from the article]

The article focuses on the limited eligibility of older adults in the early stages of Alzheimer's disease (AD) for newly approved antiamyloid drugs due to medical conditions or neuroimaging findings. It discusses only 8-17 percent of amyloid-positive individuals with early AD would be eligible for lecanemab; and 5-9 per cent for aducanumab; and highlighting the challenges in treating those with mild cognitive impairment or mild dementia with elevated brain amyloid.

The article offers information on a blood biomarker that measures astrocyte reactivity, which may help identify cognitively unimpaired older adults with amyloid-beta pathology who are at risk of developing Alzheimer's disease (AD). The study found that those with a combination of amyloid-beta burden and abnormal astrocyte activation were more likely to progress to AD, suggesting that testing for both brain amyloid and blood biomarkers of astrocyte reactivity may be an optimal screening method.

The article focuses on a meta-analysis of Magnetic resonance imaging (MRI) data from clinical trials, suggesting that anti-amyloid-beta drugs used in the management of Alzheimer's disease may accelerate brain atrophy. The study found that different classes of these drugs can lead to the loss of brain and hippocampal volume, as well as an increase in ventricular volume, raising concerns about the long-term effects on brain health.

The article focuses on the uncertainty surrounding the relevance of brain volume reductions in the context of therapeutic treatment for amyloids. It discusses about the need for longer observation periods to determine if brain volume losses continue or decrease and the importance of clinical outcomes regardless of Magnetic resonance imaging (MRI) changes, according to an accompanying editorial.

The article reports that the blood test called PrecivityAD, developed by C₂N Diagnostics, can be used to identify people who show no symptoms, with an increased possibility of having a protein brain amyloid which can cause Alzheimer's Disease.

The article reports on the theory about the Alzheimer's disease and viruses in which scientists are previously skeptical on the idea. It cites on the evidence that viruses might involved in Alzheimer's disease with two types of herpes. The article also reports on the development and progress of the disease as the viruses could start an immune response resulted to the accumulation of amyloid.

The article discusses the work of Alzheimer's disease researcher Dr. Claude Wischik. While many of his peers believe the protein beta amyloid is the primary cause of Alheimer's, Wischik has spent years trying to demonstrate that a protein called tau is at fault. Details are presented about experiments that have cast doubt on the beta-amyloid theory, and lent a measure of support to Wischik's views. INSET: Signs of Decline.

The article discusses a test developed by drug company Eli Lilly & Co. and approved by the U.S. Food and Drug Administration that can detect amyloid proteins on the brain that are associated with Alzheimer's disease. The Lilly test involves administering the chemical florbetapir, which adheres to the proteins and can be detected via positron emission tomography.

The article focuses on the Anti-Amyloid in Asymptomatic Alzheimer (A4) Study which funded by the National Institute on Aging. It highlights the prevalence of Alzheimer's disease among the African Americans or American people. It cites the improtance of medical education about Alzheimer's disease particularly for the aging African Americans.

The article offers information on the testing of three drugs to prevent Alzheimer's disease in people, who are tend to develop Alzheimer's. It mentions the gantenerumab drug made by Roche Holding AG and the other two drugs made by Eli Lilly and Co. It adds that gantenerumab binds to clumps of amyloid and remove it from the brain. It includes the drugs to be tested on 160 people from the U.S., Great Britain, and Australia.

The article reports on the discovery of a gene mutation that prevents Alzheimer's disease. It states that the protective mutation slows beta amyloid production that causes the brain disease. The discovery provides strong evidence that beta amyloid buildup is a driving force in this destructive brain disease.

A study of a rare gene mutation that protects people against Alzheimer's disease provides the strongest evidence yet that excessive levels of a normal brain substance, beta amyloid, are a driving force in the disease -- bolstering hopes that anti-amyloid drugs already under development might alter the disease's course or even prevent it. So far, the drugs have not succeeded. But scientists not connected with the new study said it suggested that the drug companies' big bets on anti-amyloid treatments could yet pay off. [ABSTRACT FROM AUTHOR]

The article discusses medical research as of January 2012. A study by Doctor William Jagust, published in the "Archives of Neurology" suggested that people who are mentally active beginning in childhood and remain throughout their lives develop fewer amyloid plaques. A study published in "Archives of Internal Medicine" showed that a common iodide contrast agent given to patients who undergo medical scans yearly raises the risk of thyroid disease.

Alzheimer's researchers are obsessed with a small, sticky protein fragment, beta amyloid, that clumps into barnaclelike balls in the brains of patients with this degenerative neurological disease. It is a normal protein. Everyone's brain makes it. But the problem in Alzheimer's is that it starts to accumulate into balls -- plaques. The first sign the disease is developing -- before there are any symptoms -- is a buildup of amyloid. And for years, it seemed, the problem in Alzheimer's was that brain cells were making too much of it. [ABSTRACT FROM AUTHOR]

Researchers report that a spinal fluid test can be 100 percent accurate in identifying patients with significant memory loss who are on their way to developing Alzheimer's disease. Although there has been increasing evidence of the value of this and other tests in finding signs of Alzheimer's, the study, which will appear Tuesday in the Archives of Neurology, shows how accurate they can be. The new result is one of a number of remarkable recent findings about Alzheimer's. [ABSTRACT FROM AUTHOR]

Ideas about how to treat Alzheimer's fall into two main categories. The main one pins its hopes on blocking amyloid beta peptides that form areas of plaque on the brain. But there is also another protein, tau, that is part of the disease. Tau is damaged when patients have Alzheimer's, chemically modified so it wrecks structures inside cells that are used to transport chemicals. Amyloid and plaque are easier to track. There are new scans that show plaque in the brain, while scans for tau, which forms spaghettilike tangles inside dying nerve cells, are in much earlier stages of development. [ABSTRACT FROM PUBLISHER]

The article reports on new Alzheimer's disease research. Scientists are beginning to emphasize a multi-faceted approach to treating and preventing Alzheimer's among patients who are genetically susceptible to the disease. The author discusses how previous medical research focused almost exclusively on amyloid plaques; these plaques build up in individuals who eventually develop Alzheimer's.

Focuses on a debate between medical researchers and scientists at the 9th International Conference on Alzheimer's Disease about the origins of the disease and how to treat it. Three different views on the disease's origins; Doubt that amyloid is the cause; Development of many therapies that may be harmful if they target amyloid; Description of amyloids and what they do; Agreement by all that there is still no cure for the disease.

Focuses on the resistance of leading researchers in the Alzheimer's field to consider causes other than the "amyloid hypothesis." Results of research conducted by Dr. Jie Shen, a molecular geneticist and neurobiologist at Harvard Medical School, suggesting that amyloid is not the cause of Alzheimer's disease; Indication of resistance to Shen's work when she attempted to get her research published in medical journals; Comments from one of the Harvard scientists, who worked on the research, regarding people in the field unwilling to consider research that questions the amyloid hypothesis.

Reports on the discovery of chemicals which can reverse the toxic effects of the protein, amyloid in the brains of those with Alzheimer's disease, by Bruce A. Yankner, a researcher in the neurology department at Harvard University Medical School and colleagues at the University of Alaska. Growth factor function of amyloid; Evidence that amyloid interacts with certain chemical messengers and brain-cells.

Reports on the research of the role of the protein called amyloid, which overendows the brains of people with Alzheimer's disease, by Tom Thomas, Micheal Mullan and their collegues at the University of South Florida. Role of amyloid; Impact of an overabundant amyloid in Alzheimer's patients; Comments from Mullan.