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Category: neuroscience

Consciousness: Philosophers & Neuroscientists Defend Physicalism

In this video, leading philosophers and neuroscientists defend the view that the mind purely physical?
Starring some of the very experts who anti physicist quote such as Bob Kirk (Zombie argument) and Frank Jackson (Marys room argument) who have now turned to physicalism, as well as the most cited neuroscientists in the world, Karl Friston and other leading scholars such as Ned Block, David Papineau, Richard Brown, Ken Williford, Anil Seth and Marc Solms, we examine the strongest case for physicalism—the view that everything about the mind can ultimately be explained in terms of the physical brain.

We take on some of the most famous anti-physicalist arguments, including: The Hard Problem of Consciousness, Knowledge arguments (e.g., Mary’s Room), Philosophical zombies Dualist intuitions about the self and panpsychism.

Do these arguments really show that consciousness is non-physical—or do they rely on misconceptions about how the brain works?

This video breaks down complex ideas into clear, rigorous explanations while challenging some of the most popular objections to physicalism.

If you’re interested in philosophy of mind, consciousness, neuroscience, or the nature of reality itself, this is for you.

00:00 Introduction

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Association of an Aquaporin-4 Haplotype With Cognition, Brain Volume, and Dementia Risk in Community-Dwelling Individuals Without Dementia

The findings from this study found that carrying the minor allele at an AQP4 haplotype was associated with better verbal episodic memory, larger hippocampal volumes, lower amounts of brain free water, and lower dementia risk.

Background and Objectives.

The immunoproteasome disturbs neuronal metabolism and drives neurodegeneration in multiple sclerosis

Now online! The immunoproteasome disturbs neuronal metabolism and drives neurodegeneration in multiple sclerosis: (Cell 188, 4567–4585.e1–e12; August 21, 2025)

Now online! (Cell 188, 4567–4585.e1–e12; August 21, 2025)

During post-publication review of our article, we, the authors, identified several errors in figure assembly and annotation affecting representative images and sample size reporting. These issues are limited to figure presentation and do not affect the underlying data, quantification, or conclusions of the study.

In Figure 2G, incorrect representative images were inadvertently used for the interferon-γ-OE and PSMB8-OE glutamate conditions. The correct images have now been inserted.

Automated Imaging Differentiation for DementiaIncluding Alzheimer Disease Dementia and Dementia With Lewy Bodies

Two most common causes of dementia in older adults are Alzheimer disease dementia (ADD) and dementia with Lewy bodies (DLB).1,2 Differentiating between ADD and DLB in the clinical environment remains challenging with high rates of misdiagnosis using the current standard of care.2 Up to 50% of neuropathologically confirmed DLB, known as Lewy body disease (LBD), are correctly diagnosed antemortem, with ADD as the most common misdiagnosis.2,3 Distinguishing DLB from ADD is a vital part of patient care as DLB has a worse prognosis and requires different treatment plans compared with ADD.4 Patients with DLB are particularly sensitive to neuroleptics prescribed in dementia care, leading to worsening cognitive and motor functions.5 Further, new disease-modifying therapies are approved for ADD, but not for DLB.6,7

The National Institute on Aging and Alzheimer’s Association developed a research framework for Alzheimer disease (AD) classification using biomarkers such as amyloid, tau, and neurodegeneration.8 Amyloid positivity, as assessed using PET or biofluid assays (e.g., AB42/40, ptau217), is a core pathologic, distinguishing feature of AD. However, amyloid and Lewy body copathologies occur in over 50% of patients with LBD and can contribute to diagnostic uncertainty.2,9,10 In lieu of a DLB biomarker classification framework, current diagnostic criteria recommend combining indicative and supportive biomarkers to improve distinguishing between DLB and ADD. Indicative biomarkers include dopamine transporter scans (DaTscan), myocardial scintigraphy, and polysomnography. Supportive biomarkers are collected using MRI, PET, or SPECT scans, and EEG. Current MRI biomarkers in DLB leverage the relative sparing of the medial temporal lobe (MTL) to aid in differentiation.

Fat cells steer flies away from pathogen-tainted food through a newly revealed neural circuit

If humans or animals eat something that causes them to feel unwell, they subsequently avoid this food source. Until now, it has been unclear precisely how this avoidance learning takes place. A new study shows that communication between the brain cells and fat cells could play a crucial role here. The participants from the Universities of Bonn and Tohoku (Japan) and University Hospital Bonn have revealed the previously unknown mechanism in the fruit fly Drosophila. It may also exist in a similar form in mammals and even in humans. The results have now been published in the journal Neuron.

Anyone who’s ever had an upset stomach after eating a bad meatball knows just how much this experience can put you off them. Within research, this is also known as “conditioned taste aversion”: The brain registers the immune response to the bacteria and their toxins and concludes from this that the food source should be avoided in the future.

It is not yet known how the immune system’s discovery of the pathogens leads to a change in behavior. “As this learned food avoidance can be found in all species, we investigated this question in a model organism – the fruit fly Drosophila,” explains Prof. Dr. Ilona Grunwald Kadow. “Within this model, we can clarify how the brain and body interact with each other to trigger an avoidance reaction that is vital for survival.”

Fat-producing enzyme may amplify damage in Parkinson’s disease

As the flies aged, they developed Parkinson’s-like symptoms – including impaired movement and loss of brain cells – mirroring key aspects of disease progression seen in humans.

Using large-scale genetic screening made possible by the fruit fly model, the researchers systematically identified genes involved in α-synuclein-induced toxicity. Among these, the gene mino stood out for its strong effects on disease-related symptoms, leading the team to investigate its role further. This gene codes for the enzyme glycerol-3-phosphate acyltransferase (GPAT) and plays a key role in regulating fat metabolism in cells.

When the scientists reduced the activity of the mino gene, the flies experienced less loss of brain cells, improved movement, and healthier activity patterns. In contrast, increasing the gene’s activity worsened the flies’ symptoms.

The researchers then explored whether blocking GPAT could help counter these toxic effects. They tested a compound called FSG67, which blocks the activity of GPAT and has previously been studied in laboratory settings for obesity-related and metabolic disorders.

When the flies were treated with FSG67, the harmful effects of α-synuclein – including protein clumping and fat damage – were reduced. The scientists observed similar protective effects in mouse brain cells grown in the laboratory.

Going forward, the scientists will focus on further validating these findings and exploring the possibility of developing GPAT inhibitors as a new class of drugs for Parkinson’s disease. ScienceMission sciencenewshighlights.

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The subtle science behind safer brain implants

In a recent publication appearing in Advanced Science, researchers at the Netherlands Institute for Neuroscience challenge the assumptions surrounding the design and materials used for brain implants. Softer, flexible implants are gentler than older ones, but they are not completely harmless. By carefully studying these effects, researchers can begin to design safer implants, and bring long-term, reliable implants closer to reality.

In laboratories around the world, scientists are working on a bold goal: restoring blindness using brain implants. But behind the futuristic promise lies a quieter, more complicated story about materials, assumptions, and the limits of what we really understand about the brain.

One part of this story includes a deceptively simple question: How do you place a foreign object in the brain without evoking a reaction?

Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders

Mitochondria make essential contributions to neural development. Zhao and colleagues provide an overview of the mechanisms that regulate mitochondrial biogenesis, degradation, remodelling and transport, the importance of these processes for neural development and the proposed links between altered mitochondrial dynamics and neurodevelopmental disorders.

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