Glymphatic-Lymphatic interaction in health and brain injury
Speaker: Associate Professor Rashad Hussain
Department of Neurosurgery
Medicine Institute for Neuroscience Discovery (UM-MIND)
University of Maryland School of Medicine
Glymphatic-Lymphatic interaction in health and brain injury
The brain relies on a highly coordinated fluid-clearance network to maintain extracellular homeostasis and eliminate metabolic waste. The glymphatic system facilitates cerebrospinal fluid–interstitial fluid exchange along perivascular pathways, while downstream meningeal and cervical lymphatic vessels collect and transport brain-derived fluid, macromolecules, and cellular waste toward the systemic circulation. Under physiological conditions, this coordinated transport supports fluid balance and removal of potentially neurotoxic proteins; disruption of meningeal or cervical lymphatic drainage has been associated with impaired clearance and accumulation of amyloid-β and pTau. Our work suggest that traumatic brain injury resulted and impairment of this glymphatic–lymphatic functioning and augment neuropathology. Following TBI, glymphatic transport is rapidly suppressed and can remain impaired for months, indicating that injury produces both acute and persistent disturbances in brain fluid homeostasis. Importantly, post-traumatic cerebral oedema appears to arise from failure of fluid efflux through glymphatic and associated lymphatic pathways. TBI markedly reduces transport through cervical lymphatic vessels, decreasing vessel contraction, tracer velocity, and lymphatic volume flow. These findings identify cervical lymphatic vessels as an active downstream component of brain clearance rather than a passive terminal drainage route. A major mechanism linking brain injury to simultaneous glymphatic and lymphatic dysfunction is the post-traumatic noradrenergic surge. Excessive noradrenaline suppresses glymphatic transport while directly impairing cervical lymphatic pumping by reducing contraction frequency and amplitude and disrupting coordinated contraction-wave entrainment. Consequently, fluid and neural debris accumulate within the injured brain, promoting cerebral edema, neuroinflammation, and chronic pathological protein deposition leading to AD/ADRD.
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Neuroscience seminars at the QBI play a major role in the advancement of neuroscience in the Asia-Pacific region. The primary goal of these seminars is to promote excellence in neuroscience through the exchange of ideas, establishing new collaborations and augmenting partnerships already in place.
Seminars in the QBI Auditorium on Level 7 are held on Wednesdays at 12-1pm, which are sometimes simulcast on Zoom (with approval from the speaker). We also occassionally hold seminars from international speakers via Zoom. The days and times of these seminars will vary depending on the time zone of the speaker. Please see each seminar listed below for details.
