Beta-Amyloid Protein Buildup Linked to Anxiety, Depression in Older People, Study Finds

Beta-Amyloid Protein Buildup Linked to Anxiety, Depression in Older People, Study Finds

Increased amounts of beta-amyloid proteins often lead to worse anxiety symptoms in cognitive healthy, older individuals, according to a study published in The American Journal of Psychiatry.

The study, “Longitudinal Association of Amyloid Beta and Anxious-Depressive Symptoms in Cognitively Normal Older Adults” supports the hypothesis that emerging symptoms like anxiety and depression can be a precursor of preclinical Alzheimer’s disease in elderly people.

Alzheimer’s is a neurodegenerative disease characterized by the progressive accumulation of toxic proteins, such as beta-amyloid and tau, in the brain. The accumulation process may start more than a decade before the first manifestations of brain function decline, designated as preclinical stage of the disease.

Previous studies have suggested that anxiety and depression contribute to Alzheimer’s, and that these and other neuropsychiatric symptoms could help predict Alzheimer’s progression during early stages of the disease.

To better understand the association between brain beta-amyloid proteins and depression symptoms, a team led by researchers from Boston’s Brigham and Women’s Hospital evaluated the clinical records of 270 older individuals with no reported cognitive impairment or active psychiatric disorders.

The clinical data came from the Harvard Aging Brain Study, an observational study to improve knowledge of changes due to early Alzheimer’s.

The team determined depression scores based on the 30-item Geriatric Depression Scale and the evaluation of three cluster symptoms of depression: apathy-anhedonia (inability to experience pleasure), dysphoria (profound generalized dissatisfaction) and anxiety. Researchers analyzed scores over a five-year period.

Combined with brain imaging data, the depression scores revealed that higher amounts of beta-amyloid in the brain were associated with increasing anxiety symptoms over time. The team believes that this finding suggests that worsening anxiety-depressive symptoms can be an early predictor of beta-amyloid deposition and consequently Alzheimer’s disease progression.

“Rather than just looking at depression as a total score, we looked at specific symptoms such as anxiety,” Dr. Nancy Donovan, a geriatric psychiatrist at Brigham and Women’s and lead author of the study, said in a press release. “When compared to 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.”

She added: “If further research substantiates anxiety as an early indicator, it would be important for not only identifying people early on with the disease, but also, treating it and potentially slowing or preventing the disease process early on.”

Additional studies are still needed to determine if escalating depressive symptoms can progress to clinical depression and dementia stages of Alzheimer’s over an extended time period.

One comment

  1. A likely explanation for this finding is TAU build up in the axons of neurons of the locus coeruleus, leading to anxiety (associated with the locus coeruleus) and depression (noradrenergic deficit), while the beta-amyloid build up is probably a closely related side-effect, not involved in causing the symptoms. Thus, an association with beta-amyloid, but not evidence that beta-amyloid causes the symptoms. Tau build-up in the locus coeruleus is probably the earliest measurable change in the progression of Alzheimer’s disease. No progress will be made in understanding or treating Alzheimer’s disease until it is understood that beta-amyloid is not in the causal chain leading to Alzheimer dementia, but APOE genotype (which is also associated with elevated beta-amyloid in the brain but decrease in the CSF) is.

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