Alzheimer’s disease (AD) is a neurodegenerative disease and the primary cause of dementia in people above the age of 60. AD is characterized by a decline in thinking and independence in personal daily activities. The presence of amyloid aggregates and tau protein fibrils are the primary pathological features of AD.
Dementia with Lewy bodies (DLB) is the second most common neurodegenerative disease with dementia. DLB is characterized by the pathological accumulation of alpha-synuclein aggregates, cognitive changes in attention and alertness, visual hallucinations, reduced dopamine transporter uptake, and Parkinsonian syndrome. Frontotemporal dementias (FTD) regroup dementias with atrophy in frontal and temporal areas and display symptoms in behavior and language. Expansion repeats in c9orf72 and mutations in TDP43 have been linked to FTD.
Dementia is considered a multifactorial disease. Several risk factors such as increasing age, genetic factors, head injuries, vascular diseases, infections, and environmental factors play a role in the disease. As a multifactorial disorder, the effects of external and internal risk factors act collectively to affect common processes resulting in an acceleration of the rate of aging that is the ultimate cause of the disease. Lifestyle changes that aim to reduce the impact of these processes are therefore a credible strategy to slow the rate of aging and the risk of dementia.
A clear association of neurotoxicants with dementias has been reported. Amyloid beta (Ab), neurofibrillary tangles (NFTs), oligomers of alpha-synuclein, or c9orf72-linked toxic dipeptide repeats are associated with neuronal stress in dementias. A plethora of evidence supports the notion that many neurotoxicants such as heavy metals, pesticides, antimicrobials, and environmental pollutants, are directly connected to the pathological progression of dementias. Nevertheless, investigations are needed to better understand the potential mechanisms to address these neurotoxicants and improve approaches to their risk exposure that aid in the pathogenesis of these diseases.
This Research Topic will explore the role of all neurotoxicants in the molecular mechanisms of the pathogenicity of dementias.
We welcome the submission of original research articles and reviews to provide a better understanding of the comprehension of their role in the progression of dementias. We also welcome any putative new innovative treatment that could counteract their negative action in the pathogenesis of dementia, including Alzheimer’s disease, Lewy bodies dementia, and frontotemporal dementia.
Dr. Kevin Hascup consults for Kisbee Therapeutics. All conflicts are managed by the Office of Compliance at SIU School of Medicine. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Alzheimer’s disease (AD) is a neurodegenerative disease and the primary cause of dementia in people above the age of 60. AD is characterized by a decline in thinking and independence in personal daily activities. The presence of amyloid aggregates and tau protein fibrils are the primary pathological features of AD.
Dementia with Lewy bodies (DLB) is the second most common neurodegenerative disease with dementia. DLB is characterized by the pathological accumulation of alpha-synuclein aggregates, cognitive changes in attention and alertness, visual hallucinations, reduced dopamine transporter uptake, and Parkinsonian syndrome. Frontotemporal dementias (FTD) regroup dementias with atrophy in frontal and temporal areas and display symptoms in behavior and language. Expansion repeats in c9orf72 and mutations in TDP43 have been linked to FTD.
Dementia is considered a multifactorial disease. Several risk factors such as increasing age, genetic factors, head injuries, vascular diseases, infections, and environmental factors play a role in the disease. As a multifactorial disorder, the effects of external and internal risk factors act collectively to affect common processes resulting in an acceleration of the rate of aging that is the ultimate cause of the disease. Lifestyle changes that aim to reduce the impact of these processes are therefore a credible strategy to slow the rate of aging and the risk of dementia.
A clear association of neurotoxicants with dementias has been reported. Amyloid beta (Ab), neurofibrillary tangles (NFTs), oligomers of alpha-synuclein, or c9orf72-linked toxic dipeptide repeats are associated with neuronal stress in dementias. A plethora of evidence supports the notion that many neurotoxicants such as heavy metals, pesticides, antimicrobials, and environmental pollutants, are directly connected to the pathological progression of dementias. Nevertheless, investigations are needed to better understand the potential mechanisms to address these neurotoxicants and improve approaches to their risk exposure that aid in the pathogenesis of these diseases.
This Research Topic will explore the role of all neurotoxicants in the molecular mechanisms of the pathogenicity of dementias.
We welcome the submission of original research articles and reviews to provide a better understanding of the comprehension of their role in the progression of dementias. We also welcome any putative new innovative treatment that could counteract their negative action in the pathogenesis of dementia, including Alzheimer’s disease, Lewy bodies dementia, and frontotemporal dementia.
Dr. Kevin Hascup consults for Kisbee Therapeutics. All conflicts are managed by the Office of Compliance at SIU School of Medicine. The other Topic Editors declare no competing interests with regard to the Research Topic subject.