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Glial Cells as Emerging Therapeutic Targets in Neurodegenerative Diseases: Mechanistic Insights and Translational Perspectives

Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease, multiple sclerosis, and amyotrophic lateral sclerosis share converging mechanisms of neuronal dysfunction, including protein aggregation, oxidative stress, and chronic neuroinflammation. Glial cells, once considered passive supporters, are now recognized as central drivers of these processes, offering both pathogenic triggers and therapeutic opportunities. Yet, despite compelling preclinical evidence, the translation of glial-targeted therapies into clinical success has been limited. This review provides a critical synthesis of current knowledge by examining therapeutic strategies through the lens of their translational challenges and failures.

White matter injury may lead to neurodegeneration

The brain is equally divided into grey and white matter. Grey matter contains the brain’s processing hubs, linked by an information highway — the white matter. Although white matter damage is a defining feature of multiple sclerosis and is also seen in neurodegeneration including Alzheimer’s and Parkinson’s disease, the consequences of white matter damage are not well understood.

The team created localised damage to myelin – the main component of white matter – in a well-defined brain circuit and followed what happened over time. They found that small, localised myelin damage triggered a striking response in a connected, remote grey matter region. Neuronal activity fell, microglia – the brain’s immune cells – became activated, and connections between neurons were lost.

Crucially, these changes were not permanent. After myelin was regenerated, neuronal activity recovered, connections between neurons returned, and the inflammatory response subsided.

The study also challenges a common assumption about brain inflammation. Grey matter inflammation is traditionally viewed as harmful. But here, the team found that this transient response was part of the repair process itself. When they prevented grey matter inflammation, myelin regeneration was impaired.

Conversely, when the team blocked myelin regeneration, the grey matter response did not resolve and instead became chronic. This suggests that failed myelin regeneration may help drive the persistent low-grade inflammation seen in neurodegenerative disease. ScienceMission sciencenewshighlights.


Damage to white matter in the brain can trigger features associated with neurodegenerative disease, The researchers have discovered in a new study published in the journal Nature.

The first personalized brain repair for Parkinson’s

Parkinson’s disease has been a repetitive pattern of tremors, stiffness, slowing movement and an eventual dependence on medications that soften (but never stop) the decline. But what if that script is no longer fixed? What if the brain, instead of being carefully managed as it deteriorates, could actually be rebuilt from the patient’s own biology?

These questions are no longer purely theoretical. In early clinical data presented at the AD/PD 2026 International Conference in Copenhagen, San Diego-based biotech Aspen Neuroscience shared results suggesting an unusual finding in neurodegenerative disease: early signs of restoration [1]. Not slowing, not masking, but restoring.

At the center of Aspen’s approach is a radical idea of using the patient’s own cells as raw material to rebuild what Parkinson’s has taken away.

Brain-based index may reveal Alzheimer’s risk patterns in adults as young as 30

Over the past few decades, neuroscientists and medical researchers worldwide have been trying to leverage available health records, brain scans and other medical data to uncover biological markers associated with the onset of specific diseases or neuropsychiatric disorders. The identification of these biomarkers could help to devise new tools to predict the risk that individual patients will develop a specific condition, allowing doctors to intervene early, preventing or delaying its emergence or slowing down its progression.

Researchers at the University of Texas Health Science Center, UTHealth Houston School of Behavioral Health Sciences, Keck School of Medicine of USC, and University of Maryland School of Medicine recently devised a new brain-based index that could be used to track early risk factors that, in specific people, may lead to the development of Alzheimer’s disease (AD). AD is a progressive neurodegenerative condition that prompts the deterioration and death of brain cells, leading to progressive memory loss and a decline in mental functions. AD has very limited treatment options after the diagnosis but the brain changes that culminate in AD take decades, thus suggesting that public effort should be focused on prevention.

The researchers devised an index that could be used to quantify patterns in a person’s brain that measure the similarity to those observed in individuals diagnosed with AD and followed as a part of the research studies such as Alzheimer’s Disease Neuroimaging Initiative (ADNI). This index, introduced in a paper published in Molecular Psychiatry, was derived by performing a mega-analysis of publicly available brain imaging data collected from people with and without AD.

Inside the brains of 800 incarcerated men: High psychopathy linked to expanded brain surface area

People with high levels of psychopathic tendencies are often incapable of feeling empathy for other people. From a brain science perspective, empathy isn’t a single emotion but a multi-part neural process. It involves brain systems that help us share others’ feelings, understand their perspectives, and even mentally step into their experience.

The bigger picture is, however, still blurry as we lack large-scale studies that map how different features of brain structure link to both empathy and psychopathy, especially in incarcerated populations.

A recent study published in Biological Psychiatry Global Open Science investigated how personality is reflected in the brain by turning to something measurable—the brain’s physical structure.

Monotheism, Scepticism and new Posthuman goddesses and gods

Ancient Egypt provides an excellent historical model of a permissive, non-monotheistic society that fostered a sophisticated philosophical and religious framework. In this civilization, the pantheon was not viewed as a collection of mutually exclusive, jealous deities, but rather as multifaceted expressions of a singular, underlying cosmic order, known as Ma’at (truth, balance, and justice). Egyptian gods were not distant, transcendent lawgivers, but dynamic, immanent forces embedded within the natural and social world.

This worldview can be understood through the lens of Steve Nichols’ lost primal eye theory of mind. In various posthuman movement (1988) and related works, Nichols argues that human consciousness is not static but evolving, and that our ancestors recognized a deeper, unitive potential rather than a rigid separation between humanity and the divine. In ancient Egypt, this dynamic was expressed through the idea that the Pharaoh, and ultimately all enlightened individuals, could transcend ordinary human limitation and realize a posthuman state. Rather than being subjects of an external master, humans could merge with the cosmos, making the Egyptian model an early manifestation of the posthuman approach to mind and consciousness. Even creation of your own afterlife, using MVT ‘aware circuits’

Prof Steve Nichols, May 2026.

Scientists 3D-printed bendable soft sensors into every brain fold, opening a new path for personalized neurology

A new study has found that soft 3D-printed brain sensors can follow individual brain folds more closely than standard rigid devices.

The closer fit preserved stronger electrical readings in rats while leaving nearby brain tissue largely undisturbed in early tests.

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