ABSTRACT: A new study suggests that ISRS, commonly prescribed antidepressants, can reduce biological markers of Alzheimer’s disease. In a cohort of 191 individuals, patients with EA in SSRs had lower levels of TAU-181 phosphorylated plasma, a key indicator of the severity of the disease.
The brain scan also showed that the SSRIs restored metabolic activity in the core of the dorsal raphe (DRN), an early site of Tau accumulation and serotonin production. This metabolic recovery was not observed in healthy individuals, which suggests a specific effect of the disease.
Key facts:
Reduced TAU biomarkers: EA patients in the SSRIs had significantly lower levels of P-TAU181, a tau pathology blood based. Highlighting brain activity: The SSRIs reversed hypometabolism in the nucleus of the dorsal raphe, a region rich in serotonin and the early site of Alzheimer’s damage. complicating conclusions about functional benefit.
Source: Neuroscience News
A new study suggests that selective serotonin reuptake inhibitors (SSRIs), a common class of antidepressants, can do more than a mood: they could help reduce the biological load of Alzheimer’s disease (AD).
Researchers have found that the use of long -term SSRs in patients with EA is associated with a reduced TAU pathology, a distinctive seal of the disease and activity restored in a key brain region, although the effects on memory and cognition remain complex.
The nucleus of the dorsal raphe (DRN), a small region in the brain trunk, is one of the earliest areas to show the accumulation of Tau in AD. It is also the main source of serotonin of the brain, the neurotransmitter directed by the SSRIs.
This new research shows that in people with Alzheimer’s, the DRN becomes metabolically slow, but the treatment with SSRIs seems to reverse this, which increases its activity towards healthy levels.
The research team analyzed the data of 191 participants in the Neuroimaging initiative of Alzheimer’s disease (ADNI), comparing individuals with and without use of ISRs.
They measured a blood biomarker of Tau pathology (TAU-181 phosphorylated or P-TAU181), made brain scanns of metabolic activity and evaluated cognitive performance in different tests.
They discovered that EA patients who used SSRs had P-TAU181 plasma levels in plasma than those who do not take antidepressants. These results suggest a possible protective effect of SSRs on Tau pathology.
Brain images confirmed that DRN in patients with EA is typically hypometabolic, essentially little active.
However, patients with SSRs showed glucose metabolism restored in this region, a revivated neuronal function sign. This effect was specific to those with AD; Healthy control participants showed no changes in DRN’s metabolism with the use of SSRIs, possibly due to a feedback regulation incorporated in the serotonin system that cushions unnecessary activity.
Despite these promising biological findings, the impact of the SSRIs on cognitive performance was mixed.
While some patients performed better in certain cognitive tests (such as the cognitive evaluation of Montreal, or MOCA), others did not show measurable improvements.
Interestingly, the usual correlation between the different cognitive evaluations was broken in SSR users, which implies that antidepressants can affect the way in which cognitive deterioration is measured, instead of how it progresses.
Researchers emphasize that this was a transversal study, which means that it cannot prove the cause and effect. Nor could he account for the specific types or doses of the SSRs used, or if the treatment began before or after the symptoms of the EA arose.
Even so, these results offer strong support for additional clinical trials that explore the moment, duration and cognitive impact of ISRs treatment on neurodegenerative diseases.
In summary, this study adds to the growing evidence that the brain serotonin system is deeply intertwined with Alzheimer’s pathology.
Although the SSRIs are mainly prescribed for mood disorders, they can also influence the key processes in Alzheimer’s, including the metabolism of vulnerable brain regions and the spread of toxic proteins.
As researchers continue to investigate the connection between mood, memory and chemistry of the brain, SSRIs can offer a surprising ally in the fight against cognitive deterioration.
About this neuropharmacology and the research news of Alzheimer’s disease
Author: Neuroscience News Communications
Source: Neuroscience News
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Original research: open access.
“The SSRIs reduce plasma tau and restore the metabolism of the dorsal raphe in Alzheimer’s disease” by Dylan J. Terstege et al. Alzheimer’s and dementia
Abstract
The SSRIs reduce plasma tau and restore the metabolism of the dorsal raphe in Alzheimer’s disease
INTRODUCTION
Tau pathology impacts neurodegeneration and cognitive decline in Alzheimer’s disease (AD), with the core of the dorsal raphe (DRN) between the brain regions that show TAU’s earliest pathology. As a serotonergic center, DRN activity is altered by selective serotonin reuptake inhibitors (SSRs), which also have variable effects on cognitive deterioration and pathology in the EA.
Methods
We examine n = 191 subjects with transmission tomography of Plasma Postitrones 18f-Fluorodeoxiglucosa and data from Plasma Biomarkers to study the effects of SSRIs on Tau pathology, cognitive deterioration and Drn metabolism.
RESULTS
TAU 181 Plasma phosphorylated (P-TAU181) was lower with the use of SSRI. The effect of SSRS on cognition varied according to cognitive evaluation. DRN was hypometabolic in patients with EA in relation to healthy controls; However, the use of SSRI restored the metabolic activity of this region in patients with EA.
DISCUSSION
The use of long -term SSRs can reduce the pathological presentation of the EA but has variable effects on cognitive performance.
