"“This study reveals that ALS is not a single event but a domino-like cascade that begins inside motor neurons with TDP-43 pathology and is then amplified by a damaging immune response in the bloodstream and spinal cord,” said co-corresponding author David Gate, PhD, director of the Abrams Research Center on Neurogenomics and assistant professor of Neurology in the Division of Behavioral Neurology."
"“The intensity of spinal cord inflammation doesn't determine when someone develops ALS - it determines how fast the disease progresses and how long they survive,” said co-corresponding author Evangelos Kiskinis, PhD, associate professor of Neurology in the Division of Neuromuscular Disease and of Neuroscience. “If we can target these immune signatures therapeutically, we can slow down the rate of disease progression.”"
"The study found immune cells converge at sites of motor neuron loss and TDP‑43 pathology - a hallmark of ALS - with distinct inflammatory patterns depending on the type of ALS (genetic or non-genetic, the most common form) and how quickly the disease progresses."
"Using cutting-edge techniques, the scientists analyzed blood and spinal cord samples from almost 300 patients - l"
ALS survival varies widely after symptom onset. A cascade model links early TDP-43 pathology inside motor neurons to later damaging inflammatory responses. Immune cells accumulate at sites of motor neuron loss and TDP-43 pathology. Inflammatory patterns differ by ALS subtype, including genetic versus non-genetic forms and differences in progression speed. Spinal cord inflammation intensity does not determine when ALS begins, but it correlates with how quickly symptoms worsen and how long patients survive. Targeting immune signatures may slow disease progression and support more personalized treatment approaches. Blood and spinal cord samples from nearly 300 patients were analyzed to connect immune activity with disease course.
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