Research Brief: A Literature Review of Frontotemporal Dementia and Driving.

Am J Alzheimers Dis Other Demen

Gerontology Department, McCormack Graduate School of Policy and Global Studies, The University of Massachusetts Boston, Boston, MA, USA.

Published: August 2014

There is a growing body of research on Alzheimer's disease and driving, but much less is known about less common dementias, such as frontotemporal dementia (FTD). The purpose of this study was to review the empirical literature about FTD and driving. A study was included if it met the following criteria: published from 1992 to 2013 in English, research involving humans, and included both FTD and driving data. We searched the following electronic databases: EBSCOhost, PubMed, Google Scholar, Proquest, Web of Knowledge, and Publishing Connect. A total of 367 abstracts were reviewed; however, only 4 articles satisfied the inclusion criteria. Results showed that drivers with FTD had more problems than control groups. Specific driving issues were related to antisocial behaviors common among people with FTD (eg, hit and run crashes, failure to stop at red lights, speeding infractions, and failure to recognize pedestrians at intersections). More research on FTD and driving is needed.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852854PMC
http://dx.doi.org/10.1177/1533317513518656DOI Listing

Publication Analysis

Top Keywords

ftd driving
12
frontotemporal dementia
8
driving
6
ftd
6
literature review
4
review frontotemporal
4
dementia driving
4
driving growing
4
growing body
4
body alzheimer's
4

Similar Publications

The most recurrent familial cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the presence of an abnormal number of intronic GGGGCC (G4C2) repetitions in the C9orf72 gene, which has been proposed to drive ALS/FTD pathogenesis. Recently, it has been shown that such G4C2 repetitions can fold into G-quadruplex (G4) secondary structures. These G4s have been selectively stabilized by small-molecule binders, furnishing proof of principle that targeting these non-canonical nucleic acid sequences represents a novel and effective therapeutic strategy to tackle neurodegenerative disorders.

View Article and Find Full Text PDF
Article Synopsis
  • - Neurodegenerative diseases like Alzheimer's and FTD/ALS feature synaptic loss and dendritic degeneration, linked to impaired neuronal health regulated by the CREB transcription factor.
  • - The study found that neurons from patients with a specific genetic mutation exhibited reduced CREB activation, which led to poorer dendritic and synaptic health due to an imbalance in PKA subunits.
  • - By modulating cAMP levels, researchers were able to restore CREB activity, improve neuron structure, and highlight potential therapeutic targets for treating FTD/ALS and similar disorders.
View Article and Find Full Text PDF

Purpose: The loss of olfactory function is known to occur in patients suffering from (behavioral variant) frontotemporal dementia ((bv)FTD) and Alzheimer's disease (AD), although different pathophysiological mechanisms underpin this clinical symptom in both disorders. This study assessed whether brain metabolism of the olfactory circuit as assessed by positron emission tomography (PET) imaging with 2-[fluorine-18]fluoro-2-deoxy-d-glucose ([F]-FDG) can distinguish these entities in different subsets of patients.

Methods: Patients presenting with cognitive decline were included from a prospectively kept database: (1) bvFTD patients, (2) AD patients and (3) patients with logopenic primary progressive aphasia (PPA).

View Article and Find Full Text PDF

Unlabelled: Neuronal hyperexcitability is a hallmark of amyotrophic lateral sclerosis (ALS) but its relationship with the TDP-43 aggregates that comprise the predominant pathology in over 90% of ALS cases remains unclear. Emerging evidence in tissue and slice culture models indicate that TDP-43 pathology induces neuronal hyperexcitability suggesting it may be responsible for the excitotoxicity long believed to be a major driver of ALS neuron death. Here, we characterized hyperexcitability and neurodegeneration in the hippocampus of doxycycline-regulatable rNLS8 mice (NEFH-tTA x tetO-hTDP-43ΔNLS), followed by treatment with AAV encoded DREADDs and anti-seizure medications to measure the effect on behavioral function and neurodegeneration.

View Article and Find Full Text PDF

Creation of de novo cryptic splicing for ALS and FTD precision medicine.

Science

October 2024

UCL Queen Square Motor Neuron Disease Centre, Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, University College London, London WC1N 3BG, UK.

Article Synopsis
  • The study focuses on TDP-REG, a tool designed to take advantage of the specific splicing changes caused by TDP-43 loss of function (TDP-LOF), which is linked to ALS and similar neurodegenerative diseases.
  • It utilizes a deep learning algorithm, SpliceNouveau, to create customizable splicing events that enhance protein expression correlated with the disease state, both in lab settings (in vitro) and in living organisms (in vivo).
  • TDP-REG allows for targeted editing of genetic sequences, potentially correcting harmful splicing effects and leading to new precision treatment approaches for disorders related to TDP-43.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!