Disability and Poverty is a tough cycle
In PlainSpeak for Lay Audience
Disability and Poverty: A Tough Cycle
Disability and poverty are closely connected. This makes life harder for disabled people. Here’s why.
Education: Many disabled people don’t get a good education. This makes it hard for them to learn skills needed for good jobs.
Jobs: Disabled people often face problems finding jobs. There aren’t enough job opportunities, and some employers discriminate against them. Without good jobs, it’s hard to earn enough money.
Healthcare: Poor people often can’t afford good healthcare. This can lead to untreated health problems that cause or worsen disabilities.
Support Services: Disabled people need special support, like assistive devices or home modifications, but these can be expensive. Without money, they can’t get the help they need.
The National Council on Disability says that these problems make more disabled people live in poverty. The World Health Organization also says that we need to solve both poverty and disability issues together.
To break this cycle, we need to:
- Provide better education for disabled people.
- Create more job opportunities and stop workplace discrimination.
- Offer better social support services.
- Make healthcare and housing affordable and accessible for everyone.
When we invest in these areas, we help disabled people live better lives. This also helps reduce poverty and builds a stronger, fairer society for everyone.
2 versions of this post
UCLA-AIRP Answer Scholars Award
Congratulations! On behalf of the Autistic and Neurodivergent Scholars Working for Equity in Research (ANSWER) of the AIR-P, we are pleased to inform you that your project... has been selected for the 2024 ANSWER Scholars Program for the project period September 1st, 2024 – August 31, 2025. Your application, achievements, and qualifications truly impressed our review committee.
The False Moral Authority of Titles
The False Moral Authority of Titles
In today's world, holding an advanced degree or prestigious title leads those individuals to think that they are entitled to the role of moral and legal gatekeeper. Such a perspective is not only outdated but dangerously arrogant.
(This echoes the colonial mindset where the "educated colonizers" claimed ipso facto moral and legal authority over those they deemed "uneducated primitives").
One quick path to fame and relevance today is the spread of negative news, fueled by algorithms that amplify these messages. As as Sri Sri Ravi Shankar noted, humans already have a tendency to doubt the positive but not the negative. For instance, when someone says "I love you," it's often met with skepticism ("Really?"), while "I hate you" is silently accepted.
Negative news triggers larger outward reactions, whereas positive news generates internal feel-good responses that don't spread as widely. As a result, negative spins and conspiracy theories have become a quick road to staying relevant and profits in the form of online followers, book deals, speaking engagements.... which in turn helps justify the perception of them as an "expert" and the "moral authority."
This phenomenon has many parallels in the field of autism. Select groups have positioned themselves as the sole experts of autism, their way the only way, and the lone voice of morality. They effectively shut down alternative lines of research in autism or approaches by being the loudest or most powerful voice. This is accompanied by vicious attacks, harassment, and doxxing of those they consider "others." This helps maintain their positions of power, fame and profit - (Perhaps they also get a rush out of this bullying).
The irony is that existing evidence-based practices are often weaponized or misrepresented to justify their stance. Just because something isn't fully explainable or understood yet doesn't mean it should be dismissed as pseudoscience. Rather, it represents science-in-progress. Complex phenomena like autism often defy simple cause-and-effect explanations, waiting for the right methods, technologies, or even an evolution in our scientific thinking to fit neatly into an explainable model.
A 'certification degree' or Ph.D. does not make one all-knowing about a highly heterogeneous condition like autism. We are all still trying to figure autism out. If we had all the explanations and solutions, the quality of life for all autistic individuals would be infinitely better. It’s crucial to remember that science is a process, not a destination. It thrives on curiosity, openness, and the willingness to challenge existing paradigms. True progress in understanding autism, and indeed any complex phenomenon, requires humility, collaboration, and an openness to diverse perspectives.
Let's resist the allure of false authority and the spread of negativity. Instead, let's foster a culture of inquiry and respect, where every voice is heard, and every avenue of research is explored. Only then can we hope to make meaningful progress in understanding and improving the lives of those within the autism community and beyond.
The Role of Parvalbumin Neurons in Autism
A PlainSpeak version for the Lay Reader
The Role of Parvalbumin Neurons in Autism
Background
Scientists believe that a special type of brain cell called Parvalbumin (PV) interneurons (INs) may play a key role in autism. Even though autism can be caused by many different genetic and environmental factors, people with autism often show similar behaviors. This suggests that there might be a common issue in the brain across different individuals with autism (1).
Understanding the role of PV+ interneurons in autism helps us see why many symptoms of autism occur, like sensory sensitivity and seizures.
The Balance of Brain Signals
Our brains need a balance between "go" signals (excitation) and "stop" signals (inhibition) to work properly. In autism, it was first thought that there is too much excitation and not enough inhibition, leading to an imbalance. This imbalance could explain why some people with autism have seizures (4,5). However, this idea is too simple because many types of brain cells are involved in maintaining this balance.
What We Know About PV+ Cells in Autism
Researchers have found that PV+ cells in the brains of autistics are often not working as they should:
- Fewer PV+ cells: There are fewer of these cells in the brain, and they produce less of a protein called parvalbumin.
- Changes in brain waves: These cells help control brain waves called gamma oscillations. In autism, the power of these gamma waves is higher than normal.
- Reduced activity: PV+ cells show less activity in response to visual signals.
PV+ cells are the most common type of inhibitory ("stop/slow down") neuron in the brain, but other types of neurons may also be involved in autism.
Brain Excitability and Sensory Sensitivity
When PV+ cells don't function properly, the brain becomes overly excitable and synchronized, making seizures more likely. This can also cause exaggerated responses to sensory inputs, like touch or sound. For example, in a mouse model of autism, the response to whisker movement is weaker in certain brain cells.
Sensory Overload
Autistics often experience sensory overload because their brains can't tune out irrelevant information. This may be due to a failure of brain cells to adapt to continuous stimulation (2).
Visual Processing
PV+ neurons are important for fine-tuning the way we see things, helping us to distinguish between different visual inputs.
Brain Waves and Communication
Increased gamma wave activity, which is linked to sensory and communication issues, is common in autism. PV+ cells help generate these waves, and their dysfunction leads to irregular brain activity patterns (3).
2 Versions of this Post
For the Science/Academic Reader
References
- 1.Contractor, A., Klyachko, V. A., & Portera-Cailliau, C. (2021). Reduced density and activity of parvalbumin interneurons in autism. Journal of Neurodevelopmental Disorders, 13(1), 1-15.
- 2.Green, S. A., & Gu, Y. (2015). Sensory hypersensitivity in autism spectrum disorders. Current Biology, 25(18), R876-R879.
- 3.Guyon, N., & Nahmani, M. (2021). Role of parvalbumin interneurons in gamma oscillations and sensory processing in autism. Frontiers in Neuroscience, 15, 692872.
- 4. Hussman, J. P. (2001). Suppressed GABAergic inhibition as a common factor in suspected etiologies of autism. Journal of Autism and Developmental Disorders, 31(2), 247-248.
- 5. Rubenstein, J. L., & Merzenich, M. M. (2003). Model of autism: Increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2(5), 255-267.
NSF names 34 Vanderbilt students and alumni as 2024 graduate research fellows
Read at https://news.vanderbilt.edu/2024/06/17/nsf-names-34-vanderbilt-students-and-alumni-as-2024-graduate-research-fellowsJun 17, 2024
A total of 34 Vanderbilt University alumni, students and incoming students have been named National Science Foundation graduate research fellows for 2024.
The prestigious fellowship program assists exceptional graduate students pursuing research-based master’s and doctoral degrees across various fields, including science, technology, engineering, mathematics, STEM education and social sciences supported by NSF. Since its inception in 1952, the NSF GRFP has been a cornerstone of support for graduate students, providing financial aid through a $37,000 annual stipend and a $16,000 allowance for educational expenses, along with opportunities for professional growth and international research endeavors.
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Hari Srinivasan, life sciences – neurosciences
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E-I Imbalance Theory of Autism
The E-I Imbalance hypothesis posits that an imbalance between excitatory and inhibitory signaling in the brain contributes to the sensory, cognitive, and behavioral features of autism.
PlainSpeak: This idea says that a mix-up between signals that excite and calm the brain can cause the sensory, thinking, and behavior issues in autism.
Read in more detail about E-I Imbalance
Couldn't agree more about how much needs to change
Loved your talk Hari! Couldn't agree more about how much needs to change!
Monotropism and Special Interests - what you need to know
In plain language for lay audience
When we talk about autism, two important ideas often come up: monotropism and special interests. These ideas help explain how autistic people focus on things they love, but they mean slightly different things.
Monotropism is a way of thinking that means autistic people tend to focus really hard on a few things at a time. Imagine being able to dive deeply into something you’re really interested in, like a favorite hobby or subject. This can make autistic people very knowledgeable and passionate about their interests. But it can also make it tough to switch focus to other things they find less interesting.
Special Interests are those specific things that autistic people get really excited about. These can be anything from dinosaurs to trains, from art to computers. These interests often last for a long time and can bring a lot of joy and comfort. They’re a big part of who they are. Sometimes, though, other people might not understand why these interests are so important to them.
So, what’s the difference? Monotropism is about the way autistic people focus their attention, while special interests are the actual things they focus on.
Scientists think that the way autistic brains work makes this deep focus possible. It’s not just a quirky behavior – it’s how their brains process information. This means autistic people often put a lot of mental energy into their favorite things, which can make it hard to deal with tasks they don’t enjoy as much.
By understanding monotropism and special interests, we can better support autistic people. We can appreciate their focus and passion while also helping them with strategies to manage tasks they find challenging.
Two Versions of this post
Research headed to SfN 2024
My research abstract accepted at Society for Neuroscience, SfN 2024 conference.
Dear Hari Srinivasan
Thank you for submitting a Scientific Abstract for Neuroscience 2024 taking place Oct 5-9 in Chicago.
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For more on my conference experience in Oct click on the link below
Understanding the E - I Imbalance Theory of Autism
In PlainSpeak for the Lay Reader
Caveat: Always keep in mind there is no single theory that perfectly explains autism. The Excitatory-Inhibition (E-I) Imbalance idea says that a mix-up between signals that excite and calm the brain can cause the sensory, thinking, and behavior issues in autism.
What Can Cause the E-I Imbalance?
Too Much Glutamate and Overactive Exciting Neurons
Glutamate is the main chemical that makes brain cells more active. If there is too much glutamate or the exciting neurons are too active, it can make the brain overly excitable. This can cause people with autism to be very sensitive to sounds, lights, and other sensory inputs and make thinking and processing information harder.
Not Enough GABA to Calm the Brain
GABA is the main chemical that calms brain cells. In autism, there can be less GABA, problems with GABA receptors, or less active calming neurons. This means the brain doesn’t have enough calming signals to balance the exciting ones, making the E-I imbalance worse.
Problems with Exciting and Calming Neurons
Neurons are the cells in the brain that send and receive signals. Exciting neurons make other neurons more active, while calming neurons reduce activity. In autism, there might be differences in the number, function, or connections of these neurons. For example, changes in certain calming neurons can disrupt the brain’s local circuits, leading to more excitement and less calming.
Important Development Periods
The E-I balance is especially important during key development times when the brain is growing and changing rapidly. If the balance is off during these times, it can affect brain development and function in the long term. This can impact learning, memory, and the formation of proper brain connections.
Changes in Synaptic Proteins
Proteins like neuroligins and neurexins help brain cells stick together and send signals. In autism, changes or problems with these proteins can lead to abnormal connections between brain cells, affecting the E-I balance.
Ion Channel Problems
Ion channels help neurons send signals by letting ions in and out. Ions are tiny charged particles, like sodium, potassium, or calcium, that neurons need to function properly. In autism, problems with these ion channels can change how neurons send signals, affecting the E-I balance.
Problems with Synaptic Plasticity
Synaptic plasticity is the ability of connections between brain cells to get stronger or weaker over time. This is important for learning and memory. Long-term potentiation (LTP) is when these connections get stronger with activity, helping with learning new things. Long-term depression (LTD) is when these connections get weaker, which helps remove unnecessary information. In autism, problems with LTP and LTD can make it harder to learn and remember things.
Role of Supporting Brain Cells (Astrocytes and Microglia)
Astrocytes and microglia are supporting cells in the brain that help maintain E-I balance. Astrocytes manage levels of glutamate and GABA, while microglia help prune synapses during development. Pruning is like trimming a tree; it removes extra connections between brain cells to make the network more efficient. Problems with these cells can lead to too much excitation or not enough inhibition.
Genetic and Epigenetic Factors
Our genes, which are like instructions for how our body works, can influence the E-I balance. Changes in how these genes are turned on or off can also affect the brain. Many genes linked to autism affect how brain cells connect and communicate, leading to differences seen in autism.
Environmental Influences
Things in the environment, like exposure to toxins, infections, and stress during pregnancy, can impact the E-I balance. These factors can change how the brain develops and works, leading to long-term effects on brain signals.
- 2 versions of this post:
- For the Scientific/Academic Audience
- PlainSpeak / Plain Language for the Lay Reader
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