The Good-25 years of failures to develop effective AD therapies have led us to a far greater understanding of AD risk factors, pathology, subtypes and clinical progression. And the field is not holding its breath for a cure. We had become almost resigned to reducing risk, management and support. BUT… we now have disease modifying therapies (DMT’s). And we have “proof of concept”: amyloid matters. The future is rosy- it is likely new therapies will target different molecules/processes and provide even greater disease modification. We’ve done it for MS (partly) and have even made slight headway with MND. Now it is time for AD.
The Bad- there is much more to AD disease modification than removing amyloid. It is likely that this is so even if target preclinical stages. Symptomatic therapies are, at best, modestly effective. The absolute numbers of people with AD/other dementias is increasing rapidly and we have made no progress in disease modification in non-AD neurocognitive disorders.
The how- we need to identify the right patients, have sufficient infusion centres, have neuroradiologists who can detect ARIA, create funding models (don’t hold our breath with PBAC but still possible) and even convince our colleagues that current DMTs work.
And, finally, participation in research needs to be both normalized and expected- by the public, the support organizations and by clinicians, as it is with cancer and cardiovascular disease. Dementia is now the top Burden of Disease in Australia- it deserves a far greater research effort.