Photo/Illutration Brain images of individuals who developed depressive symptoms in middle to old age are taken with positron emission tomography (PET) scans, revealing the early accumulation of tau, an abnormal protein thought to cause dementia. (Provided by the National Institutes for Quantum Science and Technology)

A recent study of patients who developed bipolar disorder or depression later in life revealed that half had high concentrations of dementia-causing proteins in their brains.

The team of scientists, primarily from the National Institutes for Quantum Science and Technology (QST), said its findings suggest that a range of late-life mood disorders (LLMD) could actually be the early onset of dementia.

The study, which compared the brain scans of 52 people with LLMDs to those without, found that the patients with late-life mental health issues were much more likely to have accumulations of abnormal proteins than the control group.

These findings could lead to the development of new treatments for depression and new methods to diagnose early-stage dementia.

Dementia is believed to occur, in most cases, when abnormal proteins accumulate in the brain, impairing the healthy function of nerve cells.

Since these abnormal proteins also accumulate in some people who develop depressive symptoms in middle to old age, it had been recently theorized that people with depression may be at higher risk of dementia.

In the study, Keisuke Takahata, a chief researcher at the QST, and his colleagues used specialized positron emission tomography (PET) scanning technology to take a detailed look at protein formations in the brains of LLMD patients.

Cerebral images were taken via PET scans of 52 middle-aged and elderly individuals who had developed relatively severe depression or bipolar disorder at or after age 40. They were typically patients at university-affiliated medical centers.

Results showed that 26, or half of the subjects, had buildups of an abnormal protein variant called tau. Of these 26, 15 also had accumulations of another abnormal protein, amyloid beta.

Brain images of 47 healthy people were also recorded and examined for comparison, with deposits of tau in seven, or 15 percent, and amyloid beta confirmed in only one, or 2 percent, of the healthy group.

Examining the scans more closely, the researchers noticed that patients with particularly severe symptoms, such as hallucinations or delusions, showed a large volume of tau in their frontal lobes and other brain areas connected to mood disorders.

Taking all these factors into account, the team concluded that the abnormal proteins responsible for dementia may cause depression and other mental illnesses to manifest as an earlier stage of dementia, prior to the full onset of the memory disorder.

The scientists stressed that their hypothesis is also supported by data from a brain bank in Japan, which preserves brain tissue for research purposes.

Brain bank records show that patients with late-life-onset depression or bipolar disorder first experience symptoms seven years, on average, before receiving dementia diagnoses.

These discoveries could prove helpful for treating depression, as physicians and scientists become increasingly aware of the correlation between deteriorated psychological states and the initial effects of dementia.

New types of medicines—including lecanemab, which suppresses abnormal protein accumulation—have already been released to treat dementia, which was previously considered incurable.

Shin Kurose, a research associate at the QST, explained the program’s future course.

“We will use PET scans, which have not yet been widely adopted to treat mental disorders, to develop new treatments based on the degree of abnormal protein accumulation, and develop new methods to effectively prevent and diagnose dementia in the early stages,” Kurose said.

The team’s findings were published on June 9 in the online edition of the international academic journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association at (https://doi.org/10.1002/alz.70195).

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