The process of memory entails the activation of numerous neural networks and biochemical pathways throughout the brain. The phenomenon of memory decline in relation to aging has been the subject of extensive research for several decades. The correlation between the process of aging and memory is intricate and has various aspects to consider. Throughout the aging process, there are various alterations that take place within the brain and, as expected, affect other functions that have already been linked to memory and its function such as involving microcirculation and sleep. Recent studies provide an understanding of how these mechanisms may be interconnected through the relatively new concept of the glymphatic system. The glymphatic system is strongly correlated to sleep processes. Sleep helps the glymphatic system remove brain waste solutes. Astrocytes expand and contract to form channels for cerebrospinal fluid (CSF) to wash through the brain and eliminate waste. However, the details have not been totally elusive, but the discovery of what we call the glymphatic system enables us to connect many pieces of physiology to understand how such factors are interconnected and the interplay between them. Thus, the purpose of this review is to discuss how the glymphatic system, sleep, memory, and aging are interconnected through a network of complex mechanisms and dynamic interactions.

Advanced neuroimaging is one of the most important means that we have in the attempt to overcome time constraints and expand the use of intravenous thrombolysis (IVT). We assessed whether, and how, the prior use of advanced neuroimaging (AN), and more specifically CT/MR perfusion post-processed with RAPID software, regardless of time from symptoms onset, affected the outcomes of acute ischemic stroke (AIS) patients who received IVT. Methods. We retrospectively evaluated consecutive AIS patients who received intravenous thrombolysis monotherapy (without endovascular reperfusion) during a six-year period. The study population was divided into two groups according to the neuroimaging protocol used prior to IVT administration in AIS patients (AN+ vs. AN−). Safety outcomes included any intracranial hemorrhage (ICH) and 3-month mortality. Effectiveness outcomes included door-to-needle time, neurological status (NIHSS-score) on discharge, and functional status at three months assessed by the modified Rankin Scale (mRS). Results. The rate of IVT monotherapy increased from ten patients per year (n = 29) in the AN− to fifteen patients per year (n = 47) in the AN+ group. Although the onset-to-treatment time was longer in the AN+ cohort, the two groups did not differ in door-to-needle time, discharge NIHSS-score, symptomatic ICH, any ICH, 3-month favorable functional outcome (mRS-scores of 0–1), 3-month functional independence (mRS-scores of 0–2), distribution of 3-month mRS-scores, or 3-month mortality. Conclusion. Our pilot observational study showed that the incorporation of advanced neuroimaging in the acute stroke chain pathway in AIS patients increases the yield of IVT administration without affecting the effectiveness and safety of the treatment.

High-resolution vessel wall imaging (HR-VWI) is emerging as a tool of notable utility in the diagnosis of intracranial vessel pathology. Its role in monitoring vessel wall disease response to treatment, however, is less well-established. We report the case of a 45-year-old man with left middle and anterior cerebral artery infarcts and an National Institute of Health Stroke Scale (NIHSS) score of 2. Time-of-flight magnetic resonance angiography and digital subtraction angiography showed multifocal intracranial vessel pathology without extracranial vessel involvement. Comprehensive investigation with echocardiography and 24 hours Holter electrocardiography was unrevealing and the coagulation and routine autoimmune panel results were within normal limits. Cerebrospinal fluid showed mildly elevated protein and a diagnosis of probable primary central nervous system (PCNS) angiitis was made. The diagnosis was corroborated by intracranial HR-VWI, which showed homogenous, concentric enhancement of the left supraclinoid internal carotid artery (ICA) wall. The patient received high-dose IV methylprednisolone and cyclophosphamide. Repeat brain magnetic resonance imaging with HR-VWI at 3 and 9 months showed reduction and final resolution of vessel wall enhancement without recurrent infarcts. He has since remained clinically stable with an NIHSS score of 0 on low-dose oral glucocorticoids. Our report illustrates the utility of HR-VWI in diagnosing a case of PCNS angiitis through the demonstration of a vasculitic pattern of mural enhancement. Furthermore, it has provided evidence of disease response to treatment, assisting us in modifying treatment accordingly. Tracking disease activity and response to treatment in cases of central nervous system vasculitis can be another important use of HR-VWI in clinical practice besides assisting in establishing the diagnosis.

Papadimitropoulos GN, et al. J Clin Neurol. 2017 Apr;13(2):201-202. https://doi.org/10.3988/jcn.2017.13.2.201

A 38-year-old woman presented with left-sided ataxia and a minor ischemic lesion of the left dorsolateral medulla was found on brain MRI. Magnetic resonance angiography was unremarkable (figure 1, A–C). A 3D fat-saturated black-blood 3T T1-weighted sequence (sampling perfection with application-optimized contrast using different flip-angle evolutions [SPACE]) revealed a mural hematoma of the V3 left vertebral artery segment, along the atlas loop (figure 2, A–C, arrows). The excellent volume coverage and mural/luminal distinction characteristics of the SPACE sequence1 allowed the clear depiction of vertebral artery dissection and consequent luminal stenosis, highlighting the need for high-resolution vertebral arteries imaging, particularly in young adult stroke patients.2

The glymphatic system is a brain-wide perivascular network that facilitates cerebrospinal-fluid–interstitial-fluid exchange and the clearance of metabolic waste. Growing experimental and clinical evidence suggests that glymphatic dysfunction may represent a convergent pathophysiological feature associated with aging, neuroinflammation, and neurodegeneration, although its causal position within these processes remains unresolved. In this narrative review, we synthesize human imaging, clinical, and translational evidence implicating glymphatic dysfunction across major neurodegenerative diseases and integrate these findings with emerging data supporting its role in chronic low-grade inflammation associated with aging (“inflammaging”). We further discuss how alterations in the gut microenvironment may remotely influence glymphatic function and contribute to neurodegeneration through the gut–brain axis. Although supported by extensive preclinical evidence, studies in humans increasingly demonstrate impaired glymphatic function in several neurodegenerative disorders, most assessed using diffusion tensor imaging along the perivascular space (DTI-ALPS) index. Glymphatic dysfunction is associated with cognitive decline, motor impairment, and disease progression. Aging-related alterations in astrocytic function, aquaporin-4 polarization, blood–brain barrier integrity, and perivascular fluid dynamics provide mechanistic links between inflammaging and glymphatic failure. Gut dysbiosis may further exacerbate these processes by promoting central nervous system inflammation and vascular dysfunction. Together, these findings identify the glymphatic system as a clinically relevant pathway in neurodegeneration that may be regulated by aging-associated neuroinflammatory mechanisms involving the gut–brain axis. Finally, we discuss physiological, behavioral, and pharmacologic modulators that influence glymphatic function and propose a unified framework positioning glymphatic dysfunction as a central integrator of impaired brain clearance, with potential implications for biomarker development, clinical assessment, and disease-modifying therapeutic strategies in neurodegenerative disorders.