So might bizaxofusp's unintended killing of neuron

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So might bizaxofusp's unintended killing of neurons actually inhibit tumor growth and mitigate loss of cognition?

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Most likely not. The death of the neurons would not mitigate the expression of TSP-1 which is where the problem lies.

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Glioblastoma is the most aggressive type of glioma: a class of tumors that arise from the supportive cells, most commonly astrocytes, that surround and protect neurons in the brain.
How Some Brain Tumors Hijack the Mind to Grow

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Almost certainly reactive astrocytes in an inflammatory state.

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When the researchers recorded brain activity during simple language tasks completed by the patient (such as naming an object shown in a picture), they saw a boost of activity throughout the brain regions infiltrated by the tumor. These included areas not normally involved in speech production, suggesting that the tumor had triggered this neuroplasticity.

Specifically, the tumor appeared to have influenced neurons to make new connections in response to language in areas that normally wouldn’t produce such a response.

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The tumor damages one part of the brain and the brain tries to compensate by increasing neuronal growth elsewhere. A fairly common occurrence with brain damage. People have had entire sections of the brain destroyed with new synaptic branches arising to try and handle that which had been destroyed.

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However, these new connections didn’t function as they should. Areas of the brain that had experienced this tumor-associated neuroplasticity struggled to process uncommon words compared with areas of the brain that hadn’t been invaded by the tumor.

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Two possibilities and both could be true. New neuronal networks take time to establish memory associations and the tumor itself might inhibit memory formation.

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So, while some glioblastomas appear to be capable of boosting the growth of new neural circuits, the research team concluded, this new connectivity may actually contribute to the cognitive decline seen in people with aggressive brain tumors.

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The tumor growth itself would cause cognitive decline.

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They found that a subset of tumor cells from areas with high functional connectivity and neuronal activity had an uptick in the expression of genes involved in assembling new neural circuits. This included a sevenfold increase in expression of a gene called THBS1, which directs cells to create a protein called TSP-1. TSP-1 is normally produced by healthy astrocytes in the brain and encourages the growth of new synapses.

Overall, about 2.5% of glioblastoma cells from the samples tested expressed THBS1, and cells from areas with high functional connectivity had higher levels of THBS1 expression than areas with low functional connectivity. Microscopy techniques confirmed that a subgroup of tumor cells in areas with high connectivity produced TSP-1, and that these areas formed more new synapses.

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TSP-1 under certain circumstances can act to curb angiogenesis and increase tumor cell death. It is expressed in a variety of different type of tumor cells. In tumor cells it acts to protect the tumor cells from destruction, increases tumor cell reproduction and metastasis. TSP-1 acts to increase neuronal growth. With this increase in TSP-1 for neuronal growth the glioblastoma can take advantage of the higher expressed TSP-1 to stop the immune system from killing it, increase in size and metastasize.