Category: Alzheimer Treatment News

The genes of a Colombian woman who beat the odds might lead to a new way to tackle the disease.

A newly developed blood test for Alzheimer’s disease not only aids in the diagnosis of the neurodegenerative condition but also indicates how far it has progressed, according to a study by researchers at Washington University School of Medicine in St. Louis and Lund University in Sweden.

Clinical trial of people destined to develop early-onset Alzheimer’s disease shows eliminating amyloid from brain may prevent symptoms, supports need for confirmatory studies.

An experimental treatment appears to delay Alzheimer’s symptoms in some people genetically destined to get the disease in their 40s or 50s, according to new findings from ongoing research now caught up in Trump administration funding delays.

Using cerebrospinal fluid (CSF) collected from living patients, a team of researchers at Washington University School of Medicine in St. Louis has for the first time linked disease-related proteins and genes to identify specific cellular pathways responsible for Alzheimer’s genesis and progression. Because these proteins were gathered from CSF, they are a good proxy for activity in the brain, and several of them may be potential targets for therapies.

An analysis of cerebrospinal fluid has uncovered several proteins likely involved in the development and progression of Alzheimer’s disease.

The study, published in the journal Nature Genetics, identified more than a dozen proteins that represent potential targets for future drug therapies designed to treat the disease, shedding light on how genetics and proteins influence the neurodegeneration seen in Alzheimer’s.

Alzheimer’s disease has plagued one large Colombian family for generations, striking down half of its members in the prime of life. But one member of that family evaded what had seemed would be fate: Despite inheriting the genetic defect that caused her relatives to develop dementia in their 40s, she stayed cognitively healthy into her 70s.

Researchers at Washington University School of Medicine in St. Louis now think they know why. A previous study had reported that, unlike her relatives, the woman carried two copies of a rare variant of the APOE gene known as the Christchurch mutation. In this study, researchers used genetically modified mice to show that the Christchurch mutation severs the link between the early phase of Alzheimer’s disease, when a protein called amyloid beta builds up in the brain, and the late phase, when another protein called tau accumulates and cognitive decline sets in. So the woman stayed mentally sharp for decades, even as her brain filled with massive amounts of amyloid. The findings, published Dec. 11 in the journal Cell, suggest a new approach to preventing Alzheimer’s dementia.

…researchers at Washington University School of Medicine in St. Louis have found — in mice — that Alzheimer’s-like tau deposits in the brain lead to the accumulation of a form of cholesterol known as cholesteryl esters, and that lowering cholesteryl ester levels helps prevent brain damage and behavioral changes.

In search of ways to prevent these destructive tau tangles, researchers at Washington University School of Medicine in St. Louis have identified a key step in their development. Intervening at this step potentially could forestall the destructive cascade of events that results in brain damage, the researchers said. The findings are published Sept. 20 in the journal Molecular Psychiatry.

Patients who live in less affluent neighborhoods and those from underrepresented racial or ethnic groups are less likely than others to receive specialized care for dementia, including Alzheimer’s disease, a new study from Washington University School of Medicine in St. Louis indicates. Further, the research shows that Black people are more likely than white people to be diagnosed with dementia at a later, more advanced stage, which could contribute to inequities in access to new treatments.

Researchers at Washington University School of Medicine in St. Louis and Lund University in Lund, Sweden, have identified a form of tau that could serve as a marker to track Alzheimer’s progression. The marker also could be used by Alzheimer’s drug developers to assess whether investigational tau-based drugs – the next frontier in Alzheimer’s drug development – are effective against the disease. Such drugs theoretically would benefit people in later stages of the disease, when tau tangles play a crucial role.

If researchers could uncover and mimic whatever protects these escapees, they might develop better treatments — even preventive therapies — not only for families plagued by inherited Alzheimer’s but for everyone.

In Alzheimer’s and related neurodegenerative diseases, the brain protein tau is closely linked to brain damage and cognitive decline. A new study from researchers at Washington University School of Medicine in St. Louis indicates that T cells play a key role in tau-related neurodegeneration, a finding that suggests new treatment strategies for Alzheimer’s and related diseases.

Microglia-mediated T cell infiltration drives neurodegeneration in tauopathy