The QPRT gene (quinoidotate phosphoribosyltransferase) is crucial for the degradation of quinolinic acid, a significant metabolite in the tryptophan-nicotinamide adenine dinucleotide (NAD) biosynthetic pathway. Below is a detailed overview that expands on the provided summaries, organized according to your requests.

### 1. Associated Genes
Aside from QPRT, other genes that may be associated with its function and pathological context include:
- **QPRT** has interactions with the **SLC7A1** gene, which encodes the cysteine transporter, impacting levels of cysteine, which can affect the synthesis of neuroprotective factors.
- **KYN** (kynureninase), which also participates in kynurenine and quinolinic acid metabolism, influencing neurotoxicity.
- **NMDAR** (N-Methyl-D-aspartate receptors) due to the role of quinolinate as an NMDA receptor agonist.
- **GDH** (Glutamate dehydrogenase), as glutamate signalling in excitotoxicity is related to quinolinic acid pathways.

### 2. Aging and Age-Related Diseases
Research suggests QPRT plays a role in:
- **Alzheimer’s disease**: Quinolinate levels are elevated in Alzheimer's patients, suggesting a possible neurotoxic role linked to neurodegeneration.
- **Huntington's disease**: Impaired QPRT activity may influence the concentrations of potentially pathogenic metabolites.
- **Epilepsy**: Abnormal metabolism of quinolinic acid has been implicated in seizures and neurodegeneration related to excitotoxicity.
- **Aging**: As aging occurs, changes in tryptophan metabolism and increased oxidative stress may elevate quinolinate levels, possibly affecting cognitive functions and promoting neurodegeneration.

The relationship between QPRT and these diseases indicates that modulation of its activity could be a therapeutic target for age-related cognitive decline.

### 3. Drugs and Drug Classes
While there are no specific drug interactions widely documented for QPRT, the following classes may have relevance:
- **NMDA antagonists** (e.g., Memantine): Drugs targeting glutamatergic pathways, which may address excitotoxicity linked to elevated quinolinate levels.
- **Antioxidants**: Studies suggest that reducing oxidative stress could mitigate the toxic pathways activated by elevated quinolinic acid.
- **Neuroprotective agents** that may modulate metabolism within the kynurenine pathway can impact QPRT function indirectly.

It is advisable to keep an eye on ongoing research for novel interventions targeting QPRT or related pathways.

### 4. Pathways and Biological Processes
The QPRT gene is involved in several critical biological pathways:
- **Kynurenine Pathway**: Essential for the metabolism of tryptophan to NAD+, where QPRT contributes to the conversion of quinolinic acid to nicotinic acid.
- **Neurotransmitter Biosynthesis**: It plays a role in the balance of excitatory neurotransmitters, particularly in relation to glutamate signaling.
- **Metabolism of Quinolinic Acid**: QPRT directly facilitates the catabolism of this neurotoxic metabolite.
- **Neuroprotection**: Indirectly related, as reduced levels of quinolinic acid lead to less excitotoxicity in neurons.
- **NAD+ Biosynthesis**: By contributing to NAD+ production through the tryptophan pathway, QPRT is linked variably to cellular energy metabolism and signaling.

### Conclusion
QPRT is a vital gene involved in the metabolism of neuroactive compounds that have critical implications for neurodegenerative conditions and aging. Its enzymatic role in the kynurenine pathway and interactions with various proteins and pathways underscore its importance in neurobiology and potential avenues for therapeutics targeting excitotoxicity and neuroprotection. Research is warranted to elucidate more precise drug interactions and explore modulating QPRT's activity as a therapeutic strategy in neurodegenerative diseases.