A 57-year-old man suffered from dizziness for about one year and truncal ataxia for about one month. Magnetic resonance imaging demonstrated a cystic tumor with a homogeneously enhanced mural nodule located in the cerebellar vermis. Computed tomography angiography revealed a hypervascular nodule. These findings were compatible with hemangioblastoma. Thallium-201 single photon emission computed tomography ((201)Tl-SPECT) showed moderately high uptake in the early phase and moderately high retention in the delayed phase, whereas hemangioblastoma shows almost no retention in the delayed phase. The patient underwent total removal of the tumor. The histological diagnosis was clear cell ependymoma (CCE). CCE is a rare subtype of ependymoma, which resembles hemangioblastoma in histological and neuroimaging findings, but is considerably more aggressive. (201)Tl-SPECT can provide useful information for the preoperative differential diagnosis of infratentorial CCE and hemangioblastoma.

Download full-text PDF

Source
http://dx.doi.org/10.2176/nmc.49.608DOI Listing

Publication Analysis

Top Keywords

clear cell
8
cell ependymoma
8
hemangioblastoma thallium-201
8
thallium-201 single
8
single photon
8
photon emission
8
emission computed
8
computed tomography
8
moderately high
8
retention delayed
8

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

ECU, Perth, Western Australia, Australia.

Background: The autophagy lysosomal pathway (ALP) and the ubiquitin-proteasome system (UPS) are key proteostasis mechanisms in cells, which are dysfunctional in AD and linked to protein aggregation and neuronal death. Autophagy is over activated in Alzheimer's disease brain whereas UPS is severely impaired. Activating autophagy has received most attention, however recent evidence suggests that UPS can clear aggregate proteins and a potential therapeutic target for AD and protein misfolding diseases.

View Article and Find Full Text PDF

Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

ADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea, Republic of (South).

Background: Abnormal aggregation and accumulation of tau is a hallmark of tauopathy including Alzheimer's disease. Effective targeting of tau for therapeutic purposes requires a clear understanding of its epitope landscape with identification of a key pathogenic tau species. Despite numerous proposed and tested tau epitopes, ranging from the N-terminus to the microtubule-binding region and C-terminus, the most effective target remains elusive.

View Article and Find Full Text PDF

Background: Lyn kinase, a member of the Src family of tyrosine kinases, predominantly phosphorylates ITIM and ITAM motifs linked to immune receptors and adaptor proteins, and is emerging as a target for Alzheimer's disease (AD). The role of Lyn in TREM2-mediated microglial activation and phagocytosis, a critical pathway for clearing Aβ plaques, remains unclear and potent, selective, and brain penetrant Lyn inhibitors are unavailable. In this study, we report the characterization of Lyn kinase inhibitors from the literature as well as the establishment of an advanced virtual screening platform at the IUSM-Purdue-TREAT-AD center to identify new type II Lyn inhibitors suitable as molecular probes.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Longeveron Inc., Miami, FL, USA.

Background: Alzheimer's disease (AD) is characterized by progressive atrophy of the cerebral cortex and hippocampus, with concomitant increase in ventricular volume. Lomecel-B is a novel cell-based therapeutic approach to AD that targets neuroinflammation, microvascular dysfunction, and has the potential to stimulate endogenous tissue regeneration. We conducted MRI analysis of brain morphology in the CLEAR-MIND study, a 49-patient proof-of-concept study that tested 3 different dosing regimens of Lomecel-B vs placebo in patients with mild AD dementia.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!