37 RESULTS
COMMENT The CMS approach is reasonable. To me it looks like a compromise between stakeholders with different perspectives. In this debate were stakeholders who are willing to take their chances with an intervention of unproven efficacy and known side effects, pro
COMMENT John Trojanowski was one of those larger-than-life exemplars of a generation of AD researchers. His contributions to the field are obviously enormous and enduring. For as long as I have been attending, his input at the semiannual national ADRC meetings wa
COMMENT For better or worse, when the FDA allowed Biogen to market Aduhelm, it let the genie out of the bottle and forced stakeholders to navigate a world with a lot of unanswered questions. Patients and physicians have struggled to consider whether the upsides o
COMMENT Now we move from “What will the decision be?” to “Was this the right decision?” Over the next several years we will learn, in a real-world setting, how frequently this drug beneficially transforms the lives of the patients taking it and the lives of their
COMMENT To someone who sees bioenergetic metabolism, mitochondria, and mitochondria-related biology as sitting at the center of brain aging and Alzheimer’s disease, these are very exciting papers. There are pretty solid experimental data from animal studies that
COMMENT In any therapeutic trial, of course it is much nicer to detect a potential signal of efficacy than not to detect such a signal. The more limited that signal is, though, the more cautious we have to be in interpreting its basis. One possibility here is tha
COMMENT There are several layers to consider here. Given the contrasting Phase 3 study results, it’s hard to feel confident the active intervention attenuated the rate of decline. Had the negative study not been negative, it would still be important to consider w
COMMENT This study extends prior cell culture, sub-cellular biochemical, animal, and human studies that show presenilin 1 mutations have biological consequences. As demonstrated nicely here, the stem-cell-derived model can facilitate studies of how specific PS1 m
COMMENT This is a very creative methods-development paper that will likely fill a much-needed niche in the mitochondrial research field. Over the past few decades it has increasingly become clear that mitochondria are not equivalent between cell types. For exampl
COMMENT Loss of proteostasis occurs in neurodegenerative diseases in general, and in Alzheimer’s in particular. This phenomenon, I think, is trying to tell us something important about neurodegenerative disease mechanisms. One possibility is that proteins aggrega
COMMENT I’m always encouraged to see investigators consider the possibility that mitochondria may play a role in AD. Over the past decade, data has accumulated from a number of labs that Aβ localizes to mitochondria not only in transgenic animals and in vitro sys
COMMENT This study advances the AD biomarker field by identifying a new marker, in this case cerebrospinal fluid (CSF) mitochondrial DNA (mtDNA) levels. The authors present data that suggest CSF mtDNA changes precede CSF Aβ changes. While one must use caution whe
COMMENT This interesting study of Olmsted County residents associates clinically evident parkinsonism with brain histology. The authors clarify several points that might prove useful to clinicians as they assign final diagnoses to applicable patients. First, most
COMMENT This paper places relationships between oxidative stress, BACE, and amyloidosis within a very interesting context. In doing so, it provides insight into AD etiology. 0 rswerdlow
COMMENT In this paper, the Reddy lab presents additional evidence of an Aβ-mitochondrial nexus. They report that mitochondrial fission-fusion is imbalanced in AD subject brains and in transgenic mice expressing human mutant β APP. The human brain work is particul
