Frontotemporal dementia is a complex disorder with a wide spectrum of clinical symptoms. Personalized medicine and gene therapy are promising strategies for treatment

Abstract

Frontotemporal dementia is an uncommon and complex sickness with a wide spectrum of clinical symptoms, making drug development for the condition challenging. Frontal and temporal lobe responsibilities, as well as the level to which these activities are affected in certain diseases, contribute to clinical heterogeneity. Unfortunately, the available data on symptomatic treatments is drawn from limited case studies and RCTs, which include persons with the same FTD diagnosis. Advances in the identification of new FTD treatments demand the construction of huge clinical networks that are built on collaborative, multicenter research. One of the primary drawbacks of the present studies is the variety of the assessment instruments utilized, such as the FBI, Cambridge Behavioral Inventory, NPI, and BEHAVE-AD, some of which were not originally established for FTD but were first validated for other kinds of dementia, such as AD. The FBI was shown to have high sensitivity and specificity in discriminating between bvFTD and non-FTD, whereas the NPI score did not. The new definition of Alzheimer's disease was changed from a clinical diagnostic to a biomarker-based diagnostic, although we are still a long way from providing a scientific description of FTD. In the future, there might be an increased likelihood of recognizing symptoms or signs in clinical studies because of a revision to the criteria of FTD.Treatment techniques should be customized to individual patient subgroups or mutation carriers. Currently, as a treatment for FTD-tau, antisense oligonucleotide inhibition of MAPT, tau phosphorylation inhibition, microtubule stability, and inhibition of tau aggregation are all being investigated. It is possible to inhibit TDP-43 aggregation, enhance progranulin levels, activate the autophagy–lysosome system, or modify the ubiquitin-proteasome system in FTD-TDP. Despite these breakthroughs, the etiology and genetics of FTD remain unclear. Additional genetic pathways and loci associated with immune dysregulation and inflammation have recently been discovered, furthering the search for possible treatment targets. Also, knowing who the mutation carriers are early on allows researchers to test disease-modifying drugs earlier, when cognitive problems may still be reversible. Research gaps in the etiology and clinical characterization of FTD should be resolved, as well as the production of precise biomarkers and specialized evaluation methodologies. Desharnais and colleagues have created a checklist to assist standardize future FTD clinical trials and boost the probability of successful findings.