Hippocampal Neuron Number Is Unchanged 1 Year After Fractionated Whole-Brain Irradiation at Middle Age

Abstract

Impairment on a hippocampal-dependent learning and memory test occurs 1 year after fractionated WBI at middle age. The same WBI regimen, however, does not lead to a loss of neurons or a reduction in the volume of hippocampus.

Intracranial Metastatic Disease Spares the Limbic Circuit: A Review of 697 Metastatic Lesions in 107 Patients

“…Other studies have shown no reduction in the actual number or density of hippocampal neurons at 1 year after fractionated whole-brain irradiation, but alterations in the relative numbers of the N-methyl D-aspartate receptor subunits NR1, NR2A, and NR2B within the CA1 segment. Similar changes were not seen in the CA3 segment or dentate gyrus (12)(13). The long-term neurocognitive consequences of WBRT are well documented.…”

Whole brain radiotherapy with hippocampal avoidance and simultaneous integrated boost for brain metastases: a dosimetric volumetric-modulated arc therapy study

“…To date, the disadvantage in the use of WBRT is determined by the risk of neurocognitive decline related to radiation and recently, several analyses showed that hippocampal-dependent functions are preferentially affected by radiotherapy [29,30]. Thus, to reduce this potential risk, some experiences evaluated hippocampal sparing during WBRT-SIB, using different arc therapies [14,17,[31][32][33].…”

“…Recent analysis showed that hippocampal-dependent functions, including learning, memory and spatial information processing, are preferentially affected by radiotherapy [10,11].…”

Sparing of the Neural Stem Cell Compartment During Whole-Brain Radiation Therapy: A Dosimetric Study Using Helical Tomotherapy

“…The hippocampus is a structure that is very sensitive to irradiation, and even relatively low-dose radiation exposures have been shown to cause a significant biphasic response in this area, which consists of an initial acute loss of SGZ cells mediated by the induction of apoptosis, followed by a delayed inflammatory response characterized by the loss of hippocampal neurons, reduced neurogenesis, microglial proliferation, and N-methyl-D-aspartic acid receptor remodeling (23,(27)(28)(29)(30)(31)(32)(33)(34)(53)(54)(55)(56). This damage may be irreparable (35).…”