In two trials, moderate exercise or supplements of omega-3 fatty acids and antioxidants failed to alter the course of cognitive decline in older adults.
Three studies report that the C9ORF72 expansion prevents RNAs and proteins from shuttling properly between nucleus and cytosol.
A new report paints a stark picture of the coming wave of dementia cases and their staggering cost if prevention or treatment fails to stem the tide.
Scanning for amyloid plaques in the brain may help clinicians diagnose and manage patients with a questionable diagnosis of Alzheimer’s.
The largest trial yet of ApoE4 carriers is pioneering new protocols with increasing use of technology to reach thousands of potential participants and disclose risk information.
Prevention trials are testing new protocols for telling potential participants about their heightened risk for dementia, and exploring the psychological effect of such disclosures.
The intracellular domain of the amyloid precursor protein may alter gene expression to reduce production of Aβ.
The synaptic protein abounds in the cerebrospinal fluid of AD patients and in those in the prodromal phase of the disease.
Hexanucleotide repeats in the C9ORF72 gene cause amyotrophic lateral sclerosis and frontotemporal dementia—but how? Three research groups now offer the same answer: The mutation disrupts RNAs exiting the nucleus, and proteins trying to get in. Different manifestations of the repeats may be responsible for the traffic jam. Some findings indicated the repeat-laden transcript are to blame, while others point the finger at polydipeptides translated from those RNAs. Experts agreed the real answer may be a bit of both.
To participate in secondary prevention trials, people must learn that they are at heightened risk for Alzheimer’s disease, either because they are accumulating brain amyloid, or because they carry an ApoE4 allele. How will people handle this knowledge, and how should clinicians communicate it to minimize psychological ill effects? At AAIC, speakers outlined how the A4 trial and Alzheimer Prevention Initiative’s ApoE4 study are going about disclosure, and discussed their challenges. Preliminary data indicate that most trial participants take the news in stride, perhaps paving the way for an era in which AD risk disclosure will become part of standard medical practice. Read Alzforum’s coverage.
Amyloid—check! Neurodegeneration—check! Synaptic integrity … coming soon? The core neuropathologies of Alzheimer’s disease are reflected in cerebrospinal fluid, aiding in the diagnosis and characterization of patients. In contrast, a CSF biomarker of synaptic loss remains elusive. Research presented at this year's AAIC meeting in Washington, D.C., suggests that neurogranin may fit the bill. The synaptic protein creeps up in CSF in the mild cognitive impairment phase of AD, and maybe even before. Brain imaging measures support the idea that CSF neurogranin reflects structural brain changes. Whether it offers a read-out distinct from more-established neurodegeneration markers, such as CSF tau, will likely determine whether neurogranin finds a place in the biomarker toolkit.
Wielding a cryo-electron microscope, researchers have produced the highest-resolution structure of γ-secretase to date. The new structure of the four-subunit machine, which churns out Aβ and other substrates, brings clarity to the complex’s mishmash of 20 transmembrane domains, and suggests how specific amino acid interactions help the promiscuous enzyme snip a striking variety of substrates. A map of Alzheimer’s disease-linked mutations revealed that many line up on intramembrane helices that face the core of the secretase.
Research presented at this year's AAIC meeting in Washington, D.C., lent credence to the idea that the course of brain development in early life influences whether and how dementia manifests later on. Epidemiological, imaging, and genetic studies converged on the idea that learning disabilities linked to particular areas of the cerebral cortex, and portend certain subtypes of Alzheimer's disease. Studying these specific associations may deepen our understanding of dementia in general, scientists say.
- Martha Clare Morris on Neither Exercise Nor Supplements Boost Cognition in Two Large Studies
- Adrian Isaacs on ALS Gene Repeats Obstruct Traffic Between Nucleus and Cytoplasm
- Edward B. Lee on ALS Gene Repeats Obstruct Traffic Between Nucleus and Cytoplasm
- Sanjay Pimplikar on New WAVE in Aβ Production—AICD Tempers APP Processing
- Wim Annaert on New WAVE in Aβ Production—AICD Tempers APP Processing
- Frédéric Checler on New WAVE in Aβ Production—AICD Tempers APP Processing
- Katalin Scherer on Study Suggests Respiratory Pacemaker Reduces ALS Survival