It's because there is little progress in uncovering the mechanisms of the disease. Alzheimer's et al are tau-opathies and Parkinson's et al are synuclein-opathies. Both are degenerative and we wait for their common base in a Grand Unified Theory.

I like to view degeneration of any tissue as death due to (premature) aging. So, if we treat it, we achieve immortality by applying it to all body. This is something hard.

The "premature aging" framing makes sense, but I wonder if it risks hiding the disease-specific parts

There has been massive progress in neurodegeneration research. We now understand that the brain has a complex system for processing metabolic "trash." Like all systems it has a number of components, each of which can fail. This is why a single "silver bullet" drug will likely never exist. A multi variable systems failure can not be fixed with a single variable solution.

Alzheimer’s occurs when Amyloid/Tau debris accumulates faster than the glymphatic system can export it.

Parkinson’s occurs when α-synuclein (Lewy Bodies) accumulates because the cellular recycling system (Mitophagy) has failed.

While Choline is a critical bottleneck for Alzheimer's, Glutathione and GBA enzyme activity are the primary bottlenecks for Parkinson’s. But in both cases it depends on the person and their genetics and what matters the most. If someone is at high risk for Alzheimer's a multi-pronged approach will probably be very common. For example a post menopause woman who is not on HRT, but at high risk due to parents should be getting Choline due to the low PEMT expression, but they might have a higher risk for neuroinflammation via NLRP3 and so need to also combat that too.

To say no progress has been made is to ignore the fact that we have learned a ton about the various components of these systems and how they can break down.

Here are the two approximate decay equations that you can put into an online latex viewer.

Alzheimer's

\Psi_{AD} = \int_{0}^{t} \frac{[(\mathbf{K}_{\tau} \otimes \mathbf{K}_{A\beta}) \cdot \mathcal{I}_{NLR P 3}]}{[\mathcal{G}(Li \cdot GSK3\beta^{-1}) \cdot PRO(ER\alpha \cdot \text{PEMT}) ] \cdot \Omega_{ATP}} \cdot e^{\left( \frac{\Gamma_{\text{fibrosis}} \cdot \text{PAI-1}}{EPA \cdot \text{Natto}} \right)} \, dt

Parkinson's

\Psi_{PD} = \int_{0}^{t} \frac{[(\mathbf{K}_{\alpha\text{-syn}} \otimes \mathcal{I}_{LRRK2}) \cdot \mathcal{I}_{NLRP3}]}{[\mathcal{G}(\text{Parkin} \cdot \text{PINK1}) \cdot PRO(\text{Dopamine}_{\text{flux}})] \cdot \Omega_{ATP}} \cdot e^{\left(\frac{\Gamma_{\text{Oxidative}} \cdot \text{Iron}}{\text{Glutathione} \cdot \text{GBA}}\right)} \, dt

And for good measure here is cancer

\Psi_{Onco} = \int_{0}^{t} \frac{[ (\mathbf{M}_{mut} \otimes \mathcal{G}_{growth}) \cdot \mathcal{I}_{STAT3} ]}{ [ \mathcal{G}(p53 \cdot \text{PTEN}) \cdot PRO(\text{Anoikis}) ] \cdot \Omega_{ATP}} \cdot e^{\left( \frac{\Gamma_{hypoxia} \cdot \text{VEGF}}{\text{Repair}_{DNA} \cdot \text{Immune}_{flux}} \right)} \, dt

The point of these isn't to give an exact equation, but to make the understanding of the systems and their components radically simpler for humans to understand which can help with treatment leading to questions like "Where is the bottleneck in this patients system?”