Alzheimer’s disease (AD) is the most common form of dementia that affects cognitive and memory capabilities and daily functioning. Identified over a century ago, AD still remains a burden in society today. In 2017, it was estimated that around 45 million people worldwide suffered from AD or a related dementia. As the life expectancy of the population increases, so too does the prevalence as well as the overwhelming cost of patient care of these age-related diseases such as AD. By 2050, 160 million people globally will develop AD. This progressive dementia is characterized by extracellular amyloid-beta (Aß) plaques, intracellular neurofibrillary tangles (NFTs), brain inflammation, synaptic dysfunction, and neuronal loss – all leading to cognitive impairment. Some of these neuropathological changes are thought to occur decades before any definite clinical symptoms. However, as in other sporadic neurodegenerative diseases, multiple risk factors can be attributable to the development of the disease. Although nearly 99% of AD cases are considered sporadic, the deficient knowledge about AD etiology makes its prevention an arduous task.
Multiple risk factors have been connected to a higher incidence of dementia and AD – either unmodifiable or modifiable. Some of these putative risk factors comprise aging, the main risk factor for AD; gender; genetic factors such as apolipoprotein E4 allele; and comorbidities, including cardiovascular diseases, type II diabetes, stroke, and traumatic brain injury. Moreover, it has been suggested that some lifestyle habits can be effective on preventing or reducing the risk of cognitive decline such as physical activity, healthy diet, and quitting smoking, as they decrease mid-life hypertension, diabetes and obesity. In addition, low social engagement and education, chronic stress, altered sleep pattern, and depression are noted to be related to a higher incidence of dementia and AD. Understanding these risk factors and their intimate connection to AD in terms of molecular and cellular mechanisms is imperative to combat this relevant public health threat.
The purpose of this Research Topic is to explore and discuss new evidences of different risk factors for AD and how they contribute to disease onset and pathology progression. This collection of research and review articles will focus on discussing how to identify and modify events contributing to AD pathogenesis with the aim to avoid the development of this yet incurable, devastating disease.
Alzheimer’s disease (AD) is the most common form of dementia that affects cognitive and memory capabilities and daily functioning. Identified over a century ago, AD still remains a burden in society today. In 2017, it was estimated that around 45 million people worldwide suffered from AD or a related dementia. As the life expectancy of the population increases, so too does the prevalence as well as the overwhelming cost of patient care of these age-related diseases such as AD. By 2050, 160 million people globally will develop AD. This progressive dementia is characterized by extracellular amyloid-beta (Aß) plaques, intracellular neurofibrillary tangles (NFTs), brain inflammation, synaptic dysfunction, and neuronal loss – all leading to cognitive impairment. Some of these neuropathological changes are thought to occur decades before any definite clinical symptoms. However, as in other sporadic neurodegenerative diseases, multiple risk factors can be attributable to the development of the disease. Although nearly 99% of AD cases are considered sporadic, the deficient knowledge about AD etiology makes its prevention an arduous task.
Multiple risk factors have been connected to a higher incidence of dementia and AD – either unmodifiable or modifiable. Some of these putative risk factors comprise aging, the main risk factor for AD; gender; genetic factors such as apolipoprotein E4 allele; and comorbidities, including cardiovascular diseases, type II diabetes, stroke, and traumatic brain injury. Moreover, it has been suggested that some lifestyle habits can be effective on preventing or reducing the risk of cognitive decline such as physical activity, healthy diet, and quitting smoking, as they decrease mid-life hypertension, diabetes and obesity. In addition, low social engagement and education, chronic stress, altered sleep pattern, and depression are noted to be related to a higher incidence of dementia and AD. Understanding these risk factors and their intimate connection to AD in terms of molecular and cellular mechanisms is imperative to combat this relevant public health threat.
The purpose of this Research Topic is to explore and discuss new evidences of different risk factors for AD and how they contribute to disease onset and pathology progression. This collection of research and review articles will focus on discussing how to identify and modify events contributing to AD pathogenesis with the aim to avoid the development of this yet incurable, devastating disease.