"Research Spotlight"

Publication in Nature Communications, 2025

Cognitive decline is common following a stroke, but the underlying mechanisms are not well understood. A team of researchers have uncovered the role of place cells, and how a functional subclass of them are predictors of cognitive outcome after stroke.

Publication in Molecular Neurodegeneration, 2025

A new study reveals that the protein α-Synuclein is more prevalent in advanced Alzheimer’s disease and that it accelerates amyloid-related tau accumulation. These findings show the need to consider α-synuclein in Alzheimer’s research and treatment strategies.

Publication in Nature Communications, 2025

Atherosclerotic cardiovascular diseases, including myocardial infarction and ischemic stroke, are the leading cause of mortality worldwide. A team of researchers shows that the protein MIF-2/D-DT acts as an atypical chemokine and a non-cognate ligand of CXCR4, which helps promote the development of atherosclerosis and inflammation in blood vessels. The study improves our understanding of how inflammation in blood vessels is connected to liver problems in atherosclerotic diseases and points out potential treatment pathways.

Publication in Science Translational Medicine, 2025

The Amyloid Cascade model of Alzheimer’s disease suggests that plaques of amyloid-β (Aβ) are the primary cause of the disease and trigger other pathological changes, such as the spread of abnormal tau protein. The exact connection between amyloid and tau buildup is not clear. Researchers now found an essential piece to this puzzle: by analyzing PET and MRI imaging, they show that amyloid drives the spread of tau by evoking neuronal hyperconnectivity.

Publication in Immunity, 2025

The accumulation of amyloid-β plaques is known to initiate a pathological cascade that leads to neurodegeneration and dementia. How these plaques are formed is only partially understood. Here, we provide evidence that aggregation of Apolipoprotein E (APOE) together with amyloid-β within the lysosomal system of microglia may trigger the generation of amyloid-β plaques.

Publication in Immunology, 2024

The accumulation of amyloid-β plaques is known to initiate a pathological cascade that leads to neurodegeneration and dementia. How these plaques are formed is only partially understood. Here, we provide evidence that aggregation of Apolipoprotein E (APOE) together with amyloid-β within the lysosomal system of microglia may trigger the generation of amyloid-β plaques.

Publication in Cell Reports, 2024

Researchers conducted a study on extracellular vesicles (EVs), which are vesicles that transport bioactive molecules and deliver them to recipient cells in the brain. They have discovered that these vesicles facilitate specialized communication between different types of cells. These findings emphasize the crucial role of EVs in brain development and could potentially lead to new therapeutic approaches for treating neurological diseases in the future.

Publication in Science Immunology, 2024

Researchers have compared a type of immune cells (CD8 T cells) of monozygotic twin pairs, where one twin has MS while the other shows no signs or subclinical signs of neuroinflammation. They found specific changes indicating that CD8-positive T cells play a crucial role in the early stages of multiple sclerosis. These findings can potentially open up new therapeutic avenues and could be used to develop improved diagnostic methods.

Publication in Alzheimer’s & Dementia, 2024

Researchers from Ludwig-Maximilians-Universität (LMU) Munich, in collaboration with Monash University Melbourne, have developed a novel biomarker algorithm that differentiates rare primary 4-repeat-tauopathies from Alzheimer’s disease with unprecedented precision. This innovative approach, which combines cerebrospinal fluid analysis with PET imaging, offers new insights into disease mechanisms and paves the way for advanced clinical trials.

Publication in Immunity, 2024

The central nervous system's decreased ability to regenerate as we age limits its ability to recover after demyelinating injuries, such as MS lesions. Researchers have now discovered that through training the immune system inactive microglia can be reprogrammed, restoring their ability to repair neuronal lesions.

Publication in Nature, 2024

Recurrent strokes in the days and weeks after the initial event are a common problem in patients whose original cause was arteriosclerosis. An international team of researchers has uncovered the mechanisms underlying this process and proposed a new therapy involving DNase enzymes to break down cell-free DNA. If confirmed in humans, these findings could lead to improved stroke therapy.

Publication in Cell, 2024

A stroke not only causes immediate damage to the brain, but it can also have long-term health effects on other organs, such as the heart. In a recent study published in Cell, researchers demonstrate that persistent pro-inflammatory changes in myeloid cells after stroke play a direct role in the development of cardiac fibrosis, independent of other factors that can lead to cardiovascular issues.

Publication in Nature Communications, 2024

Researchers have established three strategies to repair the function of mutant proteins causing CARASIL – a rare, genetic form of cerebral arteriopathy that leads to early-onset stroke and dementia. Their findings open perspectives for targeted protein repair.

Publication in Nature Neuroscience, 2024

Age-related myelin damage leads to white matter inflammation, but its impact on chronic neurodegenerative diseases remains unclear. A recent study reveals that amyloidosis alone can cause age-related oligodendrocyte and myelin damage in mouse models of Alzheimer's disease. The research team discovered that CD8 T cells contribute to neurodegenerative diseases associated with amyloidosis by abnormally activating microglia, resulting in myelin damage.

Publication in Nature Neuroscience, 2024

Researchers have made significant progress in unraveling novel mechanisms of glia-to-neuron conversion. Using novel methods in epigenome profiling, they identified that a posttranslational modification of the reprogramming neurogenic transcription factor profoundly impacts epigenetic rewiring and the improvement in neuronal programming. They identified a novel protein as key player in this conversion process, namely the transcriptional regulator YingYang1 that physically interacts with the neurogenic factor to open up the chromatin.

Publication in Nature Aging, 2024

Brain endothelial cells are critical components of the blood-brain barrier. They safeguard the central nervous system and their dysfunction is related to neurodegenerative diseases. Researchers have analyzed how the proteome of brain endothelial cells changes as we age, offering important insights into brain health.

Publication in Nature Metabolism, 2024

There is growing evidence that problems with insulin signaling play an important role in the development of neurodegenerative disease, but its exact mechanisms remain unclear. Researchers in a new study focusing on mitochondrial quality control identified a metabolic switch suggesting a mechanistic connection between insulin resistance and mitochondrial dysfunction.

Publication in Nature, 2024

In patients with neuromyelitis optica (NMO), an autoimmune disorder of the central nervous system (CNS), the immune system erroneously targets the AQP4 protein through the action of antibodies and T cells. Researchers have now uncovered the role of B cells in the thymus gland in this disease: these cells play a pivotal role in instructing T cells on their target for attack.

Publication in eBioMedicine, 2024

Researchers developed a new way to research inflammatory demyelinating diseases using minipigs. Their method is called miniSWINE: Minipig Stereotactic White-matter Injection using Navigation by Electromagnetism. Their method successfully models the changes observed in demyelinating and remyelinating lesions in human patients' brain. It can thus help to develop better diagnostic tools and treatments for diseases like multiple sclerosis.

Publication in Nature Communications, 2024

A combined neuroimaging and biofluid biomarker study investigated whether synaptic changes are associated with accelerated tau spreading in Alzheimer’s disease (AD). They found that higher levels of the presynaptic protein GAP-43 speed up the spread of tau in AD. These findings are relevant for developing treatments to slow down the progression of the disease.

Publication in Neuron, 2024

Mitochondria account for essential cellular processes – from energy production (ATP) to nucleotide metabolism. Dysfunction of mitochondria can lead to neurological disorders and contribute to developing diseases associated with aging. Researchers have now uncovered the role of dysfunctional mitochondria in direct neuronal reprogramming.

Publication in Nature Medicine, 2023

Glial cells play an important role in brain injuries; they can support brain function and react to the injury. Researchers found that astrocytes, a specific type of glial cells, proliferate and acquire neural stem cell properties after brain injury.

Publication in Science Translational Medicine, 2023

The chemokine receptor CXCR4 in vascular smooth muscle cells and endothelial cells has a protective function for vessels. Researchers found a microRNA molecule that can regulate CXCR4, offering a promising starting point for new therapies.

Publication in Neurology, 2023

As Parkinson's progresses, more invasive therapies are used – for example, deep brain stimulation or pump therapies. When these no longer yield results, physicians often conclude that treatment options are exhausted. However, new research shows that such patients can still benefit from a change in treatment.

Publication in Annals of Neurology, 2023

In a recent large study, researchers found two genes associated with MS disease progression. A new study now shows that one of these genes is associated with a loss of neurons and connections between neurons: people with this gene experienced 28% more brain shrinkage than those without it.

Publication in The Lancet, 2023

Results from a clinical trial show that different blood pressure medications have differential effects on the microvascular function in people with small vessel disease. The researchers found no differences for patients with sporadic small vessel disease but did find that two specific drugs resulted in improved function of cerebral blood vessels in patients diagnosed with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) when compared to another antihypertensive drug.

Publication in The Lancet, 2023

A new method makes the signals of radioactive tracers in cells in the brain visible using positron emission tomography (PET). The method and its results are of great importance for the diagnosis and therapy development of brain tumors as well as for neurological diseases in general.