Nanotechnology-based drug delivery |
Blood–brain barrier penetration, tau/amyloid-beta targeting |
Alzheimer’s, Parkinson’s |
Liposomal encapsulation, PEG-modified nanoparticles |
Phase II (various) |
Improved brain bioavailability, reduced plaques/tangles in animal models |
Hajjo et al. (2022) [473], Saraiva et al. (2016) [474] |
Stem cell therapy |
Dopaminergic neurons, motor neurons |
Parkinson’s, ALS |
iPSCs, MSCs |
Phase I/II |
Motor symptom improvement, neuron survival post-transplant |
Takahashi et al. (2007) [475], Glass et al. (2016) [476] |
Gene therapy |
SOD1, HTT, APOE ε4 |
ALS, Huntington’s, AD |
Antisense oligonucleotides, CRISPR |
Phase I/II |
Reduced toxic protein levels, slower disease progression |
Kordasiewicz et al. (2012) [477], Bennett et al. (2019) [478] |
Pharmacogenomics |
CYP2D6, COMT, APOE ε4 |
Alzheimer’s, Parkinson’s |
Genotype-guided dosing for existing drugs |
Phase II/III |
Reduced side effects, improved therapeutic outcomes |
Singh et al. (2017) [479], Müller et al. (2015) [480] |
Microbiome modulation |
Gut–brain axis, inflammation |
Parkinson’s, Alzheimer’s |
Probiotics, prebiotics, antibiotics |
Phase I |
Reduced neuroinflammation markers, improved cognitive/motor symptoms |
Sampson et al. (2016) [481], Cattaneo et al. (2017) [482] |