🧠Surgical Depression Treatment Shows Impressive Results
If you are one of the 20 million Americans who suffer from depression, you know that the disease can be utterly draining and debilitating. To make matters worse, a startling 30% of patients with depression do not experience relief even after multiple treatment interventions. To handle these extreme cases, a handful of clinical trials apply a controversial surgical technique that has been miraculously effective at treating symptoms of severe depression.
A recent study out of the University of Texas reveals new insights into this treatment, called deep-brain stimulation (DBS), regarding both its efficacy and its physical effects on the brain. The procedure consists of identifying a circuit of the brain that appears dysfunctional, surgically inserting electrodes into the brain region where this circuit resides, and administering electrical impulses to affect neuron firing. While the surgery is FDA-approved for treating Parkinson’s, dystonia, and others, its impact on depression is still being examined. Most recently, the area of interest in DBS depression treatment has been a stretch of white matter called the superolateral medial forebrain bundle (slMFB) which links the ventral tegmental area and the prefrontal cortex. In this particular study, researchers targeted the slMFB and used PET technology to learn about the metabolic mechanisms behind the success of DBS.
Since this procedure is still experimental, the study consisted of just ten subjects who were struggling with prolonged depression. Their goals were to examine both the effectiveness and the underlying brain changes caused by DBS to the slMFB. With respect to this first objective, they found the treatment to be tremendously successful. 80% of the patients experienced a reduction in depressive symptoms that was in excess of 50% (measured on the Montgomery–Åsberg Depression Rating Scale), with an average improvement of 59% after 12 months.
The next step was to correlate these improvements with brain metabolism using PET imaging data. They found that those patients who saw improvements also saw significant reductions in the metabolism of the caudate nucleus, a brain region associated with emotion and motivation. Metabolic reductions were also seen in the mediodorsal thalamus, dorsal anterior cingulate cortex, and the left ventral prefrontal cortex. Going off of these findings, DBS appears to work by affecting the activity of these regions which are largely concerned with emotional regulation, reward, and decision-making. This aligns with the study’s findings that responsive patients show a reduction in anhedonia and a greater response to reward after DBS treatment. Scientists are still in the exciting early phases of understanding this potent depression remedy. Researchers hold out hope that larger-scale studies will be approved in the near future, and that ultimately we can truly understand the functional basis of these techniques to develop a less-invasive application of the powerful effects of DBS to save millions from one of the world’s most crippling and persistent mental diseases.
🧠Article:
“Brain metabolic changes and clinical response to superolateral medial forebrain bundle deep brain stimulation for treatment-resistant depression” (08/19/2022) - Conner, C.R., Quevedo, J., Soares, J.C. et al. Brain metabolic changes and clinical response to superolateral medial forebrain bundle deep brain stimulation for treatment-resistant depression. Mol Psychiatry (2022). https://doi.org/10.1038/s41380-022-01726-0
🧠 Soda Overconsumption Causes Brain Damage and Memory Impairment
We all know that soda is bad for our health, yet almost 50% of Americans report drinking it daily. If you didn’t already have enough reason to switch to water, recent research shows that cola-based soft drinks can be disastrous for your brain, not just your waistline.
Researchers from the University of Southern Santa Catarina in Brazil assessed the neurological effects of long-term soda consumption on rats ranging from 2 to 14 months old. The experimental group was given a choice between cola and water consumption for 67 days, while the control group only had access to water. After running behavioral tests, the hippocampus and frontal cortex of the mice were removed and studied for signs of physical change.
The researchers found that mice of all ages performed worse at a maze-based spatial memory task if they had been fed the soft drinks compared to the control. The younger soda-drinking mice experienced the biggest memory impairment. The study also demonstrated long-term soda consumption can cause oxidative stress in the brain, which is also that occurs in the case of brain aging and dementia. This stress occurs when toxic ions, released as a natural byproduct of brain metabolism, are not taken up by antioxidants. If there are more ions than antioxidants, the ions can damage cells and cause aging and illness.
One mechanisms for the observed oxidative imbalance was the reduction in the antioxidant enzymes CAT and SOD in the experimental group, which coincided with an increase in the oxidative markers thiobarbituric acid reactive substances (TBARS) and dichloro-dihydro-fluorescein diacetate (DCFH) in the hippocampus, a region involved in learning and memory. The frontal cortex, a substrate responsible for working memory and higher level cognitive functions, also showed signs of oxidative imbalance. Though younger mice experienced the largest behavior deficits after soda consumption, the physical markers of oxidative stress were present across all age groups.
From this, we can gather that consistent soda consumption can have seriously harmful effects on behavior and the brain, especially if the brain is still developing. The oxidative stress that soft drinks seem to generate is a major cause of brain aging and neurodegenerative disease, and should not be taken lightly. The next time you go to buy a Coke, consider that you may be permanently damaging your capacity for learning and memory in addition to packing on the pounds.
🧠Article:
“Long-term administration of soft drink causes memory impairment and oxidative damage in adult and middle-aged rats” (08/18/22)-Michelle Lima Garcez, Tatiani Bellettini-Santos, Gustavo Luis Schiavo, Karen Vasconcelos Calixto, Francielle Mina, Eduarda Behenck Medeiros, Gabriel Casagrande Zabot, Nathalia de Souza Pereira, Natália Baltazar do Nascimento, Débora Borges Tomaz, Maria Cecília Manenti Alexandre, Ewa Kucharska, Eduardo Pacheco Rico, Josiane Budni, Long-term administration of soft drink causes memory impairment and oxidative damage in adult and middle-aged rats,Experimental Gerontology, Volume 166, 2022, 111873, ISSN 0531-5565, https://doi.org/10.1016/j.exger.2022.111873.
🧠Reversing Alzheimer’s by Growing New Neurons
Neurogenesis, the process by which the brain produces new neurons, is a relatively new topic in neuroscience. The fact that the adult brain makes new neurons didn’t become widely embraced until the 1980s, and the functional role of these new neurons remains controversial. Although it has been shown that the birth of new neurons in the hippocampus (a brain area implicated in learning and memory) is significantly impaired in people with Alzheimer’s disease (AD), there has previously been no luck in demonstrating a causal link between reduced neurogenesis and Alzheimer’s-related memory impairment.
Researchers at the University of Illinois at Chicago sought to untangle this ambiguity in an extensive study published in the Journal of Experimental Medicine. The team took a population of AD mice and deleted the Bax gene to augment hippocampal neurogenesis in a specific mouse genotype. They then administered a spatial recognition memory task on these subjects, and found a significant improvement in performance among the mice that underwent the neuron-enhancing Bax deletion.
Though they had already shown a link between neurogenesis and memory in AD mice, the team wanted to better understand the mechanisms of this phenomenon. They used a labeling technique to find that the immature neurons that arose from neurogenesis were recruited directly into memory circuits, and that the number of new neurons in these circuits correlated directly with performance on memory tasks. The AD mice that had enhanced neurogenesis had memory circuits that more closely resembled healthy mice, and their memory was similarly improved. In the words of the team, this suggests that “augmenting neurogenesis specifically increases the number of new neurons that participate in memory acquisition.”
Interestingly, enhancing new neuron formation in AD mice also affected the morphology of mature neurons in the hippocampus. The number of dendritic spines branching off of hippocampal neurons has been shown to affect memory, and declines significantly in AD populations. The researcher found that AD mice that had undergone neurogenesis augmentation saw more dendritic spines not only on the newly born neurons, but also on the neurons that were already there before the augmentation procedure.
All of this paints a very optimistic picture when it comes to developing new methods to reverse the symptoms of Alzheimer’s disease. The study shows neurogenesis may be an effective way to treat Alzheimer’s-related memory loss by contributing to memory circuits and rescuing new and existing neurons from morphological decay. These discoveries open an exciting avenue for further research to try to combat one of the most tragic and widespread neurological diseases of our time.
🧠Article:
“Augmenting neurogenesis rescues memory impairments in Alzheimer’s disease by restoring the memory-storing neurons” (08/19/2022) - Rachana Mishra, Trongha Phan, Pavan Kumar, Zachery Morrissey, Muskan Gupta, Carolyn Hollands, Aashutosh Shetti, Kyra Lauren Lopez, Mark Maienschein-Cline, Hoonkyo Suh, Rene Hen, Orly Lazarov; Augmenting neurogenesis rescues memory impairments in Alzheimer’s disease by restoring the memory-storing neurons. J Exp Med 5 September 2022; 219 (9): e20220391. doi: https://doi.org/10.1084/jem.20220391
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