Background: Frontotemporal dementia (FTD) or Pick's disease, is the second most frequent cause of primary degenerative dementia in those between 55 and 65 years old.
Case Presentation: A 57-year-old Indonesian female reported family that six months until one year prior to the presentation of her first symptoms, the patient had problems with memory, particularly short-term memory loss, with the patient unable to remember the task she was doing on time. The electroencephalogram revealed slowing background cerebral activity and diffuse slowing activity, indicating encephalopathy diffuse moderate state. CSF showed no pleocytosis and no elevated CSF Protein, but we did not perform tau level. She underwent brain magnetic resonance imaging (MRI) because of her aggression and impulsiveness. Brain MRI was notable for bilateral frontal and temporal atrophy. Incidentally, there was the leptomeningeal enhancement of the bilateral frontotemporal lobe. The patients were administered Haloperidol 0.5 mg orally twice daily, Donepezil 5 mg oral once daily, Aripiprazole 2.5 mg once daily, and Memantine 10 mg twice daily. The patient was discharged one week after admission and was started on antiviral therapy Acyclovir 800 mg 5 times a day for 14 days. The patient had shown more cooperative and less agitative.
Discussion: We report that FTD aims to help improve effective management.
Conclusion: Awareness of FTD needs to be increased even though this case is sporadic because it does not demand the possibility of this case occurring at a young age.
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http://dx.doi.org/10.1016/j.amsu.2022.104545 | DOI Listing |
Alzheimers Dement
December 2024
Purdue University, Lafayette, IN, USA.
Background: Alzheimer's disease (AD) is the leading cause of dementia, affecting 50 million people globally. Current AD animal models mainly focus on familial or inherited AD. These models often carry the APP and PSEN gene mutations from familial AD patients, or introduce microtubule-associated protein tau (MAPT) mutations, which can cause frontotemporal dementia but are not linked to AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) denotes TDP-43 deposition in older age and is consequential for cognitive function. Currently there is no way to identify LATE-NC during life. Some forms of TDP-43 deposition in younger age, related to frontotemporal dementia (FTD), are associated with pronounced asymmetrical atrophy of the temporal lobe.
View Article and Find Full Text PDFBackground: Tauopathies are a group of neurodegenerative disorders which are characterized by the accumulation of abnormal tau protein in the brain. However, the mechanistic understanding of pathogenic tau formation and spread within the brain remains elusive. Astrocytes are major immune reactive cells in the brain and have been implicated in exacerbating tau pathology by releasing extracellular vesicles (AEVs) containing pro-inflammatory cytokines and chemokines upon activation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.
Background: Limbic-predominant age-related TDP-43 encephalopathy (LATE) has been recently recognized as a cause of dementia in the elderly. LATE and Alzheimer's disease (AD) share similar clinical presentations, and their neuropathological changes-LATE-NC and ADNC-commonly co-occur in the brains of individuals with dementia. Frontotemporal degeneration (FTLD-TDP) represents another group of TDP-43-associated neurodegenerative diseases.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Denali Therapeutics Inc., South San Francisco, CA, USA.
Background: Macrophages and microglia are myeloid cells that play critical roles in the surveillance of the local environment of the tissues in which they reside. The ability of these phagocytes to perform key functions is contingent on their capacity to sense extracellular cues and mount responses that involve chemotaxis, proliferation, cytokine secretion, and phagocytosis of various cargos for lysosomal clearance. Our overarching hypothesis is that lysosomal degradation of phagocytic cargoes is critical for the resolution of cellular/tissue damage, as well as of inflammation, and that failure to accomplish this step affects myeloid cell states and immune responses.
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