Category Archives: Brain

Racial Stigmatization & Brain Health

As stress has been found to modulate the brain’s reward response, researchers at the University of California, Santa Barbara (UCSB) conducted a study investigating the effects of discrimination and dealing with negative stigma on brain functioning. The new study revealed the negative implications of racial stereotyping on the behavior of the subcortical nucleus accumbens, an area of the brain associated with anticipation of reward and punishment. Their findings were published in a paper featured in Social Cognitive and Affective Neuroscience. 

Consequences of Racial Stigmatization 

Study author Kyle Ratner, a social psychologist, and his colleagues investigated the effect of negative stereotyping on brain processing in 40 Latinx UCSB students. Participants were randomly assigned to either stigma condition or control groups. Researchers monitored participants’ brain functioning using a functional MRI as they were shown a rapid series of eight 2-3-minute videos pertaining to childhood obesity, high school dropout rates, gang-related violence, and teenage pregnancy.

In the stigmatized group, videos discussed the topics from the Latinx community perspective, suggesting that these individuals were disproportionately affected by them. Meanwhile, the control group was shown videos as related to the general U.S. population. After watching the videos, participants were asked to complete a Monetary Incentive Delay task in which faster response times resulted in monetary rewards.

Altered Brain Functioning

According to the study’s authors, machine learning analyses indicated that incentive-related patterns differed between Latinx participants subjected to negative stereotypes and those within the control group. Researchers found that individuals in the stigma condition group were significantly slower at the task than the control group, indicating disparities linked to the framing of the videos shown.

These effects were tied to personal motivation as related to nucleus accumbens functioning, according to the study’s authors, who highlight the compounding nature of external stressors that is affecting the health of disadvantaged demographics.

“It is clear that people who belong to historically marginalized groups in the U.S. contend with burdensome stressors on top of the everyday stressors that members of non-disadvantaged groups experience,” Ratner told Medical News Today in a recent article. “For instance, there is the trauma of overt racism, stigmatizing portrayals in the media and popular culture, and systemic discrimination that leads to disadvantages in many domains of life, from employment and education to healthcare and housing to the legal system.”

As such, the latest findings implicate that stigmatizing minority populations may impact how these individuals process incentives, expanding understanding of the association between racial stereotyping and personal motivation. This has significant implications for the wellbeing and health of members of these communities and requires further research efforts.

Despite the latest evidence, the study’s authors warn against generalizing their findings as the investigation primarily focused on a singular effect of stigmatization and only evaluated college students. They plan to conduct further experiments in a larger, more diverse cohort to improve the current understanding of systemic effects of structural racism and stereotyping on affected groups and their brain functioning.

Common Class of Medications Linked to AD, MCI Risk 

Several types of medications have been linked to mild cognitive impairment and Alzheimer’s disease (AD) risk in older patients over the years. A growing body of evidence points to drugs with anticholinergic effects as particularly dangerous for certain patient demographics. Emerging results from a recent study indicate that there may be a significant association between anticholinergic medications, AD biomarkers, and the incidence of mild cognitive impairment among cognitively normal older adults.

Anticholinergic Medications

Anticholinergic drugs have been widely used for a variety of medical conditions, ranging from allergies and the common cold to the treatment of hypertension. While certain anticholinergic medications require a prescription, others can be easily purchased over the counter.

This class of medications works by blocking acetylcholine, a neurotransmitter critical for memory function, from binding to receptors on certain nerve cells thereby inhibiting parasympathetic nerve impulses, which underlie involuntary muscle movements and bodily functions.

Examining the Relationship 

A team of researchers aimed to determine whether there were any cognitive consequences of anticholinergic medications (aCH) among a group of cognitively normal older patients and whether the interactive effects of genetic and cerebrospinal fluid (CSF) Alzheimer’s disease (AD) risk factors had any influence.

Led by Alexandra Weigand at the UC San Diego School of Medicine, the team of researchers assessed 688 cognitively normal participants from the Alzheimer’s Disease Neuroimaging Initiative with a mean age of 73.5 years. None of the participants presented with any cognitive or memory problems at the time of study inception. Approximately one-third of patients was taking anticholinergic medications with an average of 4.7 aCH drugs per person. The study’s authors administered comprehensive cognitive tests annually for all participants.

Cox regression models were used to examine the risk of progression to mild cognitive impairment (MCI) over a 10-year period, while linear mixed effects models were utilized to evaluate 3-year rates of memory, executive, and language function as related to anticholinergic medication administration.

Association of Anticholinergic Drugs with AD and MCI

According to the study’s findings published in Neurology, participants with AD biomarkers who were taking anticholinergic medications were up to four times more likely to develop mild cognitive impairment than those lacking biomarkers and not taking aCH drugs. Similarly, participants who were at a genetic risk for Alzheimer’s disease who took anticholinergic medications were up to 2.5 times more likely to develop MCI than those without genetic risk factors who were not taking the medications.

Further, linear mixed effects models found that anticholinergic medications predicted a steeper slope of decline in memory and language functions. This was especially true for participants with AD risk factors, in which the effects were exacerbated.

Researchers believe that the association acts in a “double hit manner” :”In the first hit, Alzheimer’s biomarkers indicate that pathology has started to accumulate in and degenerate a small region called the basal forebrain that produces the chemical acetylcholine, which promotes thinking and memory. In the second hit, anticholinergic drugs further deplete the brain’s store of acetylcholine.” Overall, the combined effect can have a severe impact on a patient’s thinking and memory.

Clinical Implications 

The latest findings implicate an increased risk of incident MCI and cognitive decline as related to anticholinergic medications with effects significantly exacerbated in patients with existing genetic risk factors and CSF-based biomarkers. These results “underscore the adverse impact of these drugs on cognition and the need for deprescribing trials, particularly among individuals with elevated risk for AD,” the study’s authors wrote, emphasizing the importance of further evaluation to determine whether reductions in drug usage can lead to reductions in MCI progression.

However, the researchers also noted that anticholinergic medications were being taken at levels much higher than the lowest effective dose recommended for older patients; 57% of participants were taking twice the recommended dosage while 18% were taking at least four times the recommended dose.

As the findings suggest, reducing anticholinergic drug consumption may help delay age-related cognitive decline. According to senior author and associate professor at the UC San Diego School of Medicine Lisa Delano-Wood, PhD, the latest study “suggests that reducing anticholinergic drug use before cognitive problems appear may be important for preventing future negative effects on memory and thinking skills, especially for people at greater risk for Alzheimer’s disease.”

While the current evidence indicates a clear association between anticholinergic medications and cognitive effects, further research efforts are needed to determine whether these agents are able to accelerate cognitive changes or lead to the development of Alzheimer’s disease and other neurodegenerative disorders.

Living in Disadvantaged Neighborhoods Increases Risk for Brain Atrophy

Continuous scientific efforts contribute to the emergence of new information revealing the intricate complexities of neurological functions and their surprising connection to a wide range of external factors. Protecting neurological function can be made possible through the growing identification of risk factors for neurodegeneration during the aging process and can help inform new preventative protocols for dementia and cognitive decline.

The latest data suggest an association between living in a disadvantaged neighborhood and developing brain atrophy, or experiencing a decrease in the number of brain cells or connections over time. Neighborhood disadvantage functions as a social determinant of health, reflecting the education, income, employment, and quality of housing within a particular geographic area. As brain atrophy typically predisposes individuals to dementia and cognitive decline, this finding has significant implications for protecting cognitive function as individuals age.

Impact of Neighborhood on Neurological Health

Examining the impact of neighborhood socioeconomic disadvantage on brain volume in a cognitively unimpaired population, researchers conducted a study of over 950 individuals without a history of cognitive impairment in Wisconsin. In their cross-sectional study, the research team evaluated participants living in the most socioeconomically disadvantaged neighborhoods using data from the Wisconsin Registry for Alzheimer’s Prevention and the Wisconsin Alzheimer’s Disease Research Center to assess T1-weighted structural MRI scans.

At the beginning of the trial, participants were not cognitively impaired based on the National Institute on Aging-Alzheimer’s Association diagnostic criteria, however, the cohort was enriched for Alzheimer’s disease risk based on a family history of dementia.

Led by Amy J.H. Kind, MD, PhD from the University of Wisconsin, researchers calculated total hippocampal volume by combining both left and right measurements and based total brain tissue volume measures on total white and gray matter volumes. Additionally, they computed both the Area Deprivation Index – a geospatially determined index of neighborhood-level disadvantage – and cardiovascular disease risk indices for each participant. Linear regression models were used to test the relationships between neighborhood disadvantage and hippocampal and total brain tissue volume – as assessed by magnetic resonance imaging.

Neighborhood Disadvantage Linked to Loss of Brain Volume

Earlier this year, the team published their findings online in JAMA Neurology which reveal that living in socioeconomically disadvantaged neighborhoods was associated with markedly decreased hippocampal and total brain tissue volume. Other middle-aged and older adults who lived in areas with lesser disadvantage experienced comparatively lower risks of both neurological outcomes. Researchers found that individuals living in the most disadvantaged neighborhoods experienced a mean of 7 years of age-related hippocampal atrophy.

Furthermore, they also noted that men living in these neighborhoods experienced a higher risk for brain atrophy than women, although the reasons for this correlation remain unknown.

Cardiovascular risk was found to mediate the association in the case of total cerebral volume, indicating that neighborhood-level disadvantage may be associated with the two neurological outcomes via distinct biological pathways.

However, investigators acknowledged potential limitations of the trial which included the “enriched risk study cohort” – including older participants and those with a family history of dementia. They note that this population “might be particularly vulnerable to the deleterious effects of neighborhood-level disadvantage on the hippocampus.” In addition, the study’s findings reveal associations and not causality due to its cross-sectional, observational nature and require further validation.

Different from the implications of individual-level socioeconomic status on neurological function, this is the first study to reveal a robust association between neighborhood-level disadvantage and hippocampal volume, according to researchers. The latest findings indicate that neighborhood disadvantage may be associated with brain tissue volume throughout the aging process even in the absence of clinical cognitive impairment.

These results may suggest new population markers to leverage in future research studies; neighborhood-level disadvantage could be considered in clinical decision-making or used to guide public health efforts that support healthy brain aging in such geographic areas.