89 RESULTS
COMMENT In this very nice paper, Chhatwal and colleagues in the Dominantly Inherited Alzheimer’s Network report that amyloid imaging done with PiB-PET showed striking variability in participants with different PSEN1, PSEN2, and APP mutations if the mutations are
COMMENT In commenting on the first set of statements in the draft decision, it states that, “The CMS
COMMENT Plasma AB-First Sign of AD, but Tough to Measure Prospectively? At C 2 N Diagnostics (St. Louis, Missouri), we were very pleased to see at this year’s CTAD meeting the excellent progress being made in the field to incorporate blood-based biomarkers (BBBs)
COMMENT This paper convincingly shows that microglia, and their state of activation, drive a portion of the FDG-PET signal in the brain. It also shows that the FDG-PET signal correlates with microglial activation state in regions of the brain that have not underg
COMMENT This interesting study assessed the effects of the ApoE3 V236E Jacksonville variant in several ways. Previous studies have suggested that the presence of this rare variant decreases risk of AD to a similar extent as APOE2. Here, the authors further confir
COMMENT This is a very nice manuscript that reports associations between amyloid, microglial activation, and tau pathology with correlations suggesting that amyloid-related microglial activation correlates with both tau pathology and with cognitive decline. One o
COMMENT This is certainly a historic decision by the FDA to approve aducanumab under its accelerated approval pathway. There is no question that at the highest doses tested, it can decrease and remove amyloid from the brain. Much has been written about the fact t
COMMENT In this very nice work Vogel, Hansson, and colleagues found that in a large number of individuals with underlying AD pathology, four general patterns of tau pathology were observed based on tau-PET scans. These patterns were linked closely to the four typ
COMMENT Like many physicians, physician-scientists, and scientists who work on Alzheimer’s disease, my major goals for our field are to develop treatments that prevent, delay the onset of, or slow the cognitive decline that occurs in AD. In the case of EMERGE and
COMMENT This paper shows that, in a very large number of presenilin-1 E280A mutation carriers (Columbian kindred) and age-matched controls, plasma NfL is higher. Statistically, cross-sectional values begin to diverge ~22 years before expected age of onset but ass
COMMENT The compound GV-971, Sodium oligomannate, was recently tested in a people who, based on clinical criteria, had mild to moderate dementia believed to be due to Alzheimer’s disease. Over a 36-week period, participants on GV-971 performed better than placebo
COMMENT The finding that this individual with a PS1 E280A mutation did not develop symptoms of cognitive impairment due to AD until her early 70s is very intriguing. The fact that she also has the ApoE3 Christchurch mutation, has very high amyloid deposition, but
COMMENT Two interesting papers being published look at the effects of APOE genotype on different aspects of AD, in particular tau pathology and cognitive progression of disease. Bondi and colleagues studied 297 older adults without dementia being followed in ADNI
COMMENT was not enough slowing of cognitive decline. It will be difficult to comment in detail until the data
COMMENT I found both of these papers fascinating. It is convincing that rocking in the young adult humans assessed increased NREM sleep, particularly stage 3, which is where the most slow-wave activity occurs. It also increased slow-wave oscillations and fast spi
