NeuroImmunology

𝐂𝐞𝐥𝐥 𝐓𝐡𝐞𝐫𝐚𝐩𝐲 𝐢𝐧 𝐍𝐞𝐮𝐫𝐨𝐬𝐜𝐢𝐞𝐧𝐜𝐞 𝐋𝐚𝐧𝐝𝐬𝐜𝐚𝐩𝐞 🧠

With 50+ companies tackling 600+ neurological disorders, the opportunity to impact… | 17 comments on LinkedIn

The peripheral immune system communicates with the brain through complex anatomical routes involving the skull, the brain borders, circumventricular organs and peripheral nerves. These immune–brain communication pathways were classically considered to be dormant under physiological conditions and active only in cases of infection or damage. Yet, peripheral immune cells and signals are key in brain development, function and maintenance. In this Perspective, we propose an alternative framework for understanding the mechanisms of immune–brain communication. During brain development and in homeostasis, these anatomical structures allow selected elements of the peripheral immune system to affect the brain directly or indirectly, within physiological limits. By contrast, in ageing and pathological settings, detrimental peripheral immune signals hijack the existing communication routes or alter their structure. We discuss why a diversity of communication channels is needed and how they work in relation to one another to maintain homeostasis of the brain. The peripheral immune system communicates with the brain through diverse anatomical routes to shape brain physiology. Here we discuss why such diversity is needed and explore how these routes are leveraged during development and hijacked in ageing.

A comprehensive study mapped neuronal IL-1R1 (nIL-1R1) expression in the mouse brain, highlighting its role in sensory processing, mood, and memory regulation.

@BrainInflCollab: In 2017 Alina Sternberg, a psychiatrist, was hit with crushing fatigue and brain fog. Neurologists told her the symptoms were caused by depression. "No, I can enjoy my life and I know what depressi...…

The evolving pathophysiological landscape of Alzheimer’s disease (AD) research increasingly indicates an intricate interplay between the brain and the immune… | 18 comments on LinkedIn

Lymphatic-specific deletion of the Calcrl gene, encoding the CGRP receptor, alleviates facial expression of chronic migraine pain. To test whether MLVs contribute to the pathophysiology of chronic migraine pain, Calcrlfl/fl;Vegfr3CreERT2/+ (CalcrliLEC) mice with lymphatic-specific, temporal...

There is a misconception that only amyloid-targeting treatments have been studied in Alzheimer's disease. The reality is that clinical trials have evaluated… | 21 comments on LinkedIn

Immune control of brain physiology

Contrary to the classical view of immune-brain communication as a dormant system activated only during pathology, this…

In this post, I am sharing the Physiology of CSF (Cerebrospinal Fluid).

Cerebrospinal fluid (CSF) is a clear, colorless fluid that surrounds the brain and…

L’apport de l’immunologie dépasse la seule compréhension de la physiopathologie des déficits immunitaires, de l’allergie ou des maladies auto immunes mais…

Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase of SARS-CoV-2 infection, affecting approximately 10% to over 30% of those infected. It presents a significant clinical challenge, notably due to pronounced neurocognitive symptoms such as brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing to a central role of cerebromicrovascular dysfunction. This review investigates key pathophysiological mechanisms contributing to cerebrovascular dysfunction in long COVID and their impacts on brain health. We discuss how endothelial tropism of SARS-CoV-2 and direct vascular infection trigger endothelial dysfunction, impaired neurovascular coupling, and blood–brain barrier disruption, resulting in compromised cerebral perfusion. Furthermore, the infection appears to induce mitochondrial dysfunction, enhancing oxidative stress and inflammation within cerebral endothelial cells. Autoantibody formation following infection also potentially exacerbates neurovascular injury, contributing to chronic vascular inflammation and ongoing blood–brain barrier compromise. These factors collectively contribute to the emergence of white matter hyperintensities, promote amyloid pathology, and may accelerate neurodegenerative processes, including Alzheimer’s disease. This review also emphasizes the critical role of advanced imaging techniques in assessing cerebromicrovascular health and the need for targeted interventions to address these cerebrovascular complications. A deeper understanding of the cerebrovascular mechanisms of long COVID is essential to advance targeted treatments and mitigate its long-term neurocognitive consequences.

I have started the new year reading many research articles on chronic inflammation. It is incredible to me how much chronic inflammation is a driver for almost…

Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time. Multiple lines of information provided by experimental, epidemiological, neuropathological and genetic studies suggest a pathological role for innate and adaptive immune activation in this disease. Here, we review the cell types and pathological mechanisms involved in disease development as well as the influence of genetics and lifestyle factors. Given the decade-long preclinical stage of Alzheimer disease, these mechanisms and their interactions are driving forces behind the spread and progression of the disease. The identification of treatment opportunities will require a precise understanding of the cells and mechanisms involved as well as a clear definition of their temporal and topographical nature. We will also discuss new therapeutic strategies for targeting neuroinflammation, which are now entering the clinic and showing promise for patients. This Review provides an in-depth examination of how inflammation contributes to neurodegeneration in Alzheimer disease. The authors explore the impact of extrinsic factors, such as brain trauma, diet and infections, and host-intrinsic factors, such as the activity of microglial cells and other immune, vascular and neuronal cell populations, on disease development. They also highlight emerging drugs that target this inflammatory component for therapy of Alzheimer disease.