In case of neurodegenerative diseases such as Alzheimer’s disease (AD), you may start your work from the study of synapses – gaps between the nerve ends – as synaptic dysfunctions are considered as most important disorders in these diseases.
Although a great deal of work has been done on neurodegenerative diseases but they still lack fully potential “disease-modifying therapies”. Disease-modifying therapy (cures the disease as opposed to the cure of only symptoms in symptomatic treatment) may start from ‘toxin-reducing’ approach.
One of the reasons of the lack of better disease-modifying drugs is incomplete understanding of mechanisms underlying the neurodegenerative diseases. Several mechanisms/pathways have been proposed such as “accumulation of neurotoxic substances, inflammation, lipid metabolism, oxidative stress, autophagy, protein degradation and mitochondrial dysfunction” but no drug is still pointing to all these mechanisms.
For the development of potential drugs against AD, better animal models have to be developed. Not only animal models but also significant biomarkers are not present for identification of AD. Presence of biomarkers could help us to understand that how early we have to start the treatment of AD.
BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases (2013). Bai Lu, Guhan Nagappan, Xiaoming Guan, Pradeep J. Nathan & Paul Wren Nature Reviews Neuroscience DOI: 10.1038/nrn3505