Worsening Anxiety in Older Adults May Precede Alzheimer’s
Identifying factors associated with a higher risk of developing Alzheimer’s may be a key to stopping its progression.
Subtle changes in the brain occur years before an individual experiences the memory loss and severe cognitive impairment associated with Alzheimer’s disease (AD). If clinicians could detect these changes early on, interventions might be possible, according to Nancy J. Donovan, M.D., a geriatric psychiatrist and professor at Brigham and Women’s Hospital.
Nancy J. Donovan, M.D., says long-term follow-up of study participants with worsening anxiety is necessary to determine if their symptoms progress to clinical depression and/or mild clinical impairment and dementia.
Steven M. Smith
Donovan and colleagues are the authors of a study published January 12 in AJP in Advance showing that cognitively normal older adults with worsening anxiety had higher levels of amyloid beta, a brain protein implicated in Alzheimer’s.
The study builds on observational research showing that depression and other neuropsychiatric symptoms often emerge during the “preclinical” phase of Alzheimer’s—a period marked by the accumulation of deposits of fibrillar amyloid and pathological tau in a patient’s brain.
“Certain older adults with elevated amyloid have normal cognition but may experience detectable changes in emotional regulation and anxiety,” Donovan told Psychiatric News.
“Recognizing these characteristic changes may help us identify high-risk older adults and target them with AD-directed treatments or psychiatric treatments that could reduce risk of progression to cognitive impairment. For example, there are suggestions in the literature that we may be able to attenuate progression very early in AD using antidepression or antianxiety treatment.”
A total of 270 participants aged 62 to 90 underwent baseline positron emission tomography (PET) scans to measure cortical amyloid beta along with annual depression assessments based on the 30-item Geriatric Depression Scale (GDS). The team calculated total GDS scores as well as scores for three GDS item clusters: apathy-anhedonia, dysphoria, and anxiety concentration. These scores were examined over one to five years (mean: 3.8 years).
“Rather than just looking at depression as a total score, we looked at specific symptoms such as anxiety,” Donovan said in a press release. “When compared with other symptoms of depression such as sadness or loss of interest, anxiety symptoms increased over time in those with higher amyloid beta levels in the brain.”
The data were acquired from the Harvard Aging Brain Study, a longitudinal dataset designed to differentiate changes associated with “normal” aging from symptoms of preclinical Alzheimer’s dementia.
“Cross-sectional studies have generally not been able to demonstrate a significant association of high amyloid in the brain and depression, but we have been collecting data for several years, so we were able to see if high amyloid was related to increasing depressive symptoms,” Donovan told Psychiatric News. “Longitudinal analyses have greater power to address this question.”
Follow-up is necessary to determine whether escalating depressive symptoms “give rise to clinical depression and/or mild cognitive impairment and dementia associated with Alzheimer’s disease over an extended period,” she said.
Donovan and her colleagues will monitor cognitive changes in the study participants for the next five years.
“Anxiety may be a manifestation of the disease process, but it also may also be a disease-potentiating factor, so if we could treat it, we may be able to attenuate progression or reduce risk of progression,” she concluded. ■
“Longitudinal Association of Amyloid Beta and Anxious-Depressive Symptoms in Cognitively Normal Adults” can be accessed here.
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Psychiatrics News
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Published online: 15 March 2018
Published in print: March 3, 2018 – March 16, 2018
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