Memory loss not enough to diagnose Alzheimer's

Diagram of the brain of a person with Alzheimer's Disease. Credit: Wikipedia/public domain.

Relying on clinical symptoms of memory loss to diagnose Alzheimer's disease may miss other forms of dementia caused by Alzheimer's that don't initially affect memory, reports a new Northwestern Medicine study.

20 sept 2016--"These individuals are often overlooked in clinical trial designs and are missing out on opportunities to participate in clinical trials to treat Alzheimer's," said first study author Emily Rogalski, associate professor at Northwestern's Cognitive Neurology and Alzheimer's Disease Center.
There is more than one kind of Alzheimer's disease. Alzheimer's can cause language problems, disrupt an individual's behavior, personality and judgment or even affect someone's concept of where objects are in space.
If it affects personality, it may cause lack of inhibition. "Someone who was very shy may go up to grocery store clerk—who is a stranger—and try to give her a hug or kiss," Rogalski said.
This all depends on what part of the brain it attacks. A definitive diagnosis can only be achieved with an autopsy. Emerging evidence suggests an amyloid PET scan, an imaging test that tracks the presence of amyloid—an abnormal protein whose accumulation in the brain is a hallmark of Alzheimer's—may be used during life to determine the likelihood of Alzheimer's disease pathology.
In the study, the authors identify the clinical features of individuals with primary progressive aphasia (PPA), a rare dementia that causes progressive declines in language abilities due to Alzheimer's disease. Early on in PPA, memory and other thinking abilities are relatively intact.
PPA can be caused either by Alzheimer's disease or another neurodegenerative disease family called frontotemporal lobar degeneration. The presence of Alzheimer's disease was assessed in this study by amyloid PET imaging or confirmed by autopsy.
The study demonstrates that knowing an individual's clinical symptoms isn't sufficient to determine whether someone has PPA due to Alzheimer's disease or another type of neurodegenerative disease. Therefore, biomarkers, such as amyloid PET imaging, are necessary to identify the neuropathological cause, the authors said.
Northwestern scientists looked at individuals in mild stages of language loss caused by Alzheimer's disease and described their brain atrophy based on MRI scans and their results on cognitive tests.
"We wanted to describe these individuals to raise awareness about the early clinical and brain features of PPA to develop metrics which would advocate for their inclusion in clinical trials targeting Alzheimer's disease," Rogalski said. "These individuals are often excluded because they don't have memory deficits, but they share the same disease [Alzheimer's] that's causing their symptoms."
The study was published online in the journal Neurology Aug. 26.

More information: Emily Rogalski et al, Aphasic variant of Alzheimer disease, Neurology (2016). DOI: 10.1212/WNL.0000000000003165


Provided by Northwestern University

Socially Active Seniors Stay Sharp

By Crystal Phend
BOSTON, 30 may 2008-- Frequent interaction with family and friends, volunteering, and other social activities may delay age-related memory loss, researchers found.Memory declined twice as fast among adults 50 and older who were least socially active as it did among those with the most social contact, Lisa F. Berkman, Ph.D., of the Harvard School of Public Health, and colleagues reported in online in the American Journal of Public Health.These results of a large observational study "suggest that increasing social integration may be an important component of efforts to protect older Americans from memory decline," they wrote.
But it's not clear whether this effect reflects a lifetime of mentally-stimulating interaction rather than current contact, which could be boosted to potentially reduce memory loss, noted Karen A. Ertel, Sc.D., of the Harvard School of Public Health and a co-author on the paper.
Because previous studies have linked social ties to incidence of dementia and Alzheimer's disease, Dr. Berkman's group looked at the effect on memory among 16,638 men and women 50 and older who were followed longitudinally in the nationally representative Health and Retirement Study.
Biennial interviews in the study included immediate- and delayed-recall memory tests used to monitor memory loss over six years in the study.
About half of the participants reported current social interaction in three or more areas, including marriage, volunteer activity, and at least weekly contact with children, parents, or neighbors.
Memory scores at baseline in 1998 were similar between highly socially active participants and those with lower levels of social activity.
Thereafter, though, memory declined faster among those with low social scores. Memory scores declined 0.32 points per year on average with an additional 0.04-point-per-year decrease for each decrease in number of types of social interaction reported (P<0.01).
After adjustment for health status and other predictors of memory decline, older adults with the lowest levels of social interaction were predicted to average a 0.29-point decline in memory score per year compared with a 0.14-point per year decline for those with social contact in all five areas.
Each individual component of social integration showed the same significant pattern of slower memory decline for those with more social contact. Analysis by gender, education, and presence of a vascular disorder likewise showed a protective effect of socialization.
The effect of social integration "may be particularly important" for individuals with less than a high school education, who had "a particularly precipitous" decline in memory score of about one point every 3 years.
"These results suggest that low social integration puts people at risk of accelerated memory loss," the researchers said, "but it is also possible that our results were attributable to reverse causation (i.e., poor memory or memory decline causing social withdrawal)."
However, Dr. Berkman's group found no evidence of reverse causation. Exclusion of participants who may have already had some memory loss at baseline as indicated by a memory score below the 25th percentile yielded results similar to those of the overall cohort.
Likewise, memory scores among a subgroup of participants enrolled in the study in 1993 explained less than 1% of variability in social integration in 1998.
"Declines in cognitive function before baseline were unlikely to explain the observed longitudinal association," the researchers wrote.
Rather, the mechanisms may include an effect on physical health, particularly diabetes and other vascular conditions implicated in other studies in development of dementia, they speculated. "Social ties may create pressure, either through explicit reminders or implicit behavioral norms, to take care of oneself."
Other possible mechanisms might be presenting complex cognitive and memory challenges that enhance cognitive reserve and resilience or through direct neurohormonal benefits by providing a sense of purpose and emotional validation, the investigators said.
They cautioned, though, that the study was limited by its nonrandomized design, lack of inclusion of all possible types of social connections and information on quality of social contacts, and low level of data on health status.
The study was funded by the National Institute of Aging. The researchers reported no conflicts of interest.
Primary source: Journal of Public HealthSource reference:Ertel KA, et al "Effects of social integration on preserving memory function in a nationally representative US elderly population" J Public Health 2008; 98.