Finally, if γ-secretase inhibitors could speak, they might borrow a quote from Mark Twain and declare that the reports of their death have been greatly exaggerated. Immunotherapy approaches appear to have mushroomed, but many scientists remain as wary of their potential side effects as they are hopeful about their ability to remove forms of Aβ or amyloid. Outliers that buck this overwhelming trend include intranasal insulin, growth factor gene therapy, gonadotropal hormones, tau immunotherapy, and dietary supplements. The majority of them dig into some aspect of the amyloid hypothesis, but not all. The lack of validated, consensus biomarkers notwithstanding, this year’s ICAD program indicates that therapeutic approaches appear to grow exponentially at the present stage of AD research. The need for early detection is pressing, and many scientists wonder whether some drugs fail partly because they are tested too late in the disease. In fact, researchers increasingly compare the phase of diagnosed AD as we know it to terminal, metastatic cancer-the end stage of a disease that ideally should be treated years before the patient shows up at the neurologist’s door.
This early detection work reflects an emerging consensus among scientists that Alzheimer disease develops for a decade, perhaps even longer, before clinical signs become apparent. On the imaging front, news included updates on the amyloid imaging agent PIB and its use in presymptomatic carriers of familial AD mutations, as well as talks on promising new approaches such as diffusion tensor imaging and perfusion MRI to measure the degradation of the brain’s white matter that is thought to precede overt AD. Efforts ranged from imaging methods and more refined neuropsychological tests to proxy markers derived from epidemiological research on risk factors in the cardiovascular and metabolic fields. It included attempts to detect telltale fingerprints of preclinical AD in body fluids, such as innovative work on leukocyte gene expression profiles or more advanced attempts to validate known biomarkers in the cerebrospinal fluid. Research in this area has exploded compared even to as recently as 5 years ago. Others viewed the commercial presence, together with the large number of presentations on a variety of experimental therapies, as a positive sign of the field’s needed movement toward translational science as patient numbers grow inexorably.Įven a casual flick through the conference program makes clear that a large fraction of the presentations focused on a panoply of different early detection and diagnostic efforts. Some scientists grumbled about feeling crammed into a crowded poster area while the neighboring company exhibits enjoyed all the space and air that’s necessary for animated conversation. Presentations included major new developments, such as the discovery that the progranulin gene causes a form of frontotemporal dementia (see ARF related news story) as well as the discovery of a physiological function for the enzyme BACE (see ARF related news story) Smaller nuggets of news solidified emerging trends or opened up new research directions. In several dozen informal interviews in hallways, ballrooms, on escalators and shuttle buses, attendees applauded that many scientists presented unpublished data in their talks and posters. (The first ICAD conference, held 1988 in Las Vegas, hosted around 300 attendees.) The conference attracted not only a record number of attendees-just above 5,000 from 50 countries-but also a visit by Queen Sofia, whose philanthropy supports AD care and research in her country. The 10th International Conference on Alzheimer’s Disease and Related Disorders, ICAD for short, ended yesterday just outside the palatial capital of Spain.
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