11505 RESULTS
COMMENT This study adds important mechanistic insight into how astrocyte expression of different APOE isoforms can contribute to AD pathology. It is intriguing that amyloid levels in APP NL-G-F mice with APOE2 were elevated compared to APOE3. A previous study had
COMMENT This paper by Preman and colleagues provides interesting insights into the biology of astrocyte-derived APOE and how it relates to microglial activation and AD plaque pathology. While historical evidence supports APOE4 promoting plaque formation, there is
COMMENT In this study, the authors examined the pathological significance of PSEN2 in a mouse model of AD: APP knock-in mice, in which Aβ plaques accumulate, were crossed with a PSEN2 knockout or with mice that had the PSEN2 familial AD mutation, N141I, knocked i
COMMENT The PSEN2 mutation is associated with familial early onset Alzheimer’s disease and is predicted to be pathogenic, supported by evidence from transgenic animals. Previous work from Win Annaert nicely tied PSEN2 activity to late endosomes and production of
COMMENT This is another high-level study by the Annaert lab and collaborating groups in Leuven, providing numerous novel insights into how presenilin 2 (PSEN2) KO and a common familial AD PSEN2 mutation affect synapses/physiology, dystrophic neurites/plaques, end
COMMENT This manuscript directly addresses two important, but related, questions that are actively, and sometimes heatedly, discussed in meetings. 1. The neurodegenerative process is the direct driver of brain dysfunction and the disease’s debilitating symptoms.
COMMENT mass spectrometry. The authors do not comment on this issue in the article, but it would be interesting
COMMENT These interesting studies end with excellent recommendations. There is much that individuals can do to decrease the chance of dementia, and this is a cause for optimism and hope. There are also policy changes that can make a difference. This report is U.S
COMMENT of an individual, which, after all, is where medical practice is applied. One last comment. Aging is
COMMENT This could accelerate the timeline for introducing antibody therapies, but societal costs, including high drug prices and resource utilization, must be carefully weighed against the clinical and societal benefits. Even if amyloid-clearing immunotherapy pr
COMMENT clinical efficacy. I will preface my comments by saying I agree, in the main, with the authors that the
COMMENT Given the urgent need for primary or secondary prevention, safe interventions with negligible side effects are important. If a long-term intervention with negligible side effects results in a sustained reduction in Aβ accumulation, it should be approved b
COMMENT As a research neurologist based in Seoul, I would like to contribute my perspective on the use of biomarkers in Alzheimer’s disease diagnosis and treatment, particularly in light of the article shared here. Biomarkers versus neuropsychological tests: I fu
COMMENT The Aisen et al. Perspective article argues that robust reduction of amyloid PET signal achieved by Aβ antibody-based therapies should serve as a surrogate biomarker of clinical response for approval of such treatments. The article provides a convincing s
COMMENT It is interesting that the datasets, studies, and arguments presented in this perspective paper bring others to different conclusions, and with an equal degree of conviction. rswerdlow 0
