The number of people worldwide over 60 years of age is increasing. According to contemporary knowledge, the aging process contributes to reduce the efficiency of defense and repair systems and leads to subclinical changes in the central nervous system (CNS), including morphological and functional deterioration of brain function, progressive loss of neurons, reduced levels of neurotransmitters, excessive inflammation, disturbed vascular integrity, and an increase in the level of pathological proteins such as ß-amyloid (Aß), tau and a-synuclein (ASN).
In addition, in the aging brain the decreasing effectiveness of repair mechanisms increases the susceptibility to reactive oxygen species, neuroinflammatory processes and spontaneous mutagenesis leading to the development of age-related diseases, including dementia, depression, Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and epilepsy. Dementia and depression are common problems among the elderly, affecting respectively almost 10% and approximately 15% of people over the age of 65.
AD is the most common cause of dementia, affecting nearly half of the population over 90 years of age. AD is associated with the deposition of pathological proteins such as Aß and phosphorylated tau, which also strongly affects the regulation of synaptic transmission, having a significant impact on the onset of epileptic-like activity. Patients with a long AD history, usually longer than 3 years, may therefore have a higher risk of developing seizures or epilepsy. Epilepsy in the elderly, which appears after 60 years of age, remains asymptomatic in the vast majority, although generalized epilepsy may also rarely manifest in that age.
In the old age, additional causes of epilepsy are cerebrovascular diseases (CVD), which contribute to 30-50% of all identified cases of epilepsy after 60 years of age. Finally, aging is the most important risk factor for the development of PD, which affects about 1% of the population in age after 60 years and around 5% over the age of 85 years. It has been shown that the pathological mechanisms of this disease are associated with the deposition of Lewy bodies (LB) composed of ASN, leading to disturbances at the molecular and subcellular levels and affecting structures such as mitochondria. Both, mitochondria and antioxidant systems are also associated with brain injury upon ischemic stroke. In the aging population the number of stroke incidents increases. Stroke in the population is expected to grow by nearly 40% over the next 20 years.
Many unexplained phenomena are implied in the aging process. This Research Topic aims to elucidate the mechanisms underlying body functioning impairment, associated with change observed in normal aging, and with the old age diseases‘ development.
It covers disorders at the molecular and functional levels in old age and may help addressing the currently unanswered questions:
-whether the brain pathologies in these individuals are associated with subtle clinical deficits,
-why various brain structures’ damage present different clinical symptoms,
-which genes and molecular factors are associated with neurodegenerative transformation,
-why Aß deposits may be found in over 80 years old individuals without showing dementia signs in normal aging.
It seems that finding the cause of pathological changes in the old age may improve health and daily functioning of older people.
The number of people worldwide over 60 years of age is increasing. According to contemporary knowledge, the aging process contributes to reduce the efficiency of defense and repair systems and leads to subclinical changes in the central nervous system (CNS), including morphological and functional deterioration of brain function, progressive loss of neurons, reduced levels of neurotransmitters, excessive inflammation, disturbed vascular integrity, and an increase in the level of pathological proteins such as ß-amyloid (Aß), tau and a-synuclein (ASN).
In addition, in the aging brain the decreasing effectiveness of repair mechanisms increases the susceptibility to reactive oxygen species, neuroinflammatory processes and spontaneous mutagenesis leading to the development of age-related diseases, including dementia, depression, Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and epilepsy. Dementia and depression are common problems among the elderly, affecting respectively almost 10% and approximately 15% of people over the age of 65.
AD is the most common cause of dementia, affecting nearly half of the population over 90 years of age. AD is associated with the deposition of pathological proteins such as Aß and phosphorylated tau, which also strongly affects the regulation of synaptic transmission, having a significant impact on the onset of epileptic-like activity. Patients with a long AD history, usually longer than 3 years, may therefore have a higher risk of developing seizures or epilepsy. Epilepsy in the elderly, which appears after 60 years of age, remains asymptomatic in the vast majority, although generalized epilepsy may also rarely manifest in that age.
In the old age, additional causes of epilepsy are cerebrovascular diseases (CVD), which contribute to 30-50% of all identified cases of epilepsy after 60 years of age. Finally, aging is the most important risk factor for the development of PD, which affects about 1% of the population in age after 60 years and around 5% over the age of 85 years. It has been shown that the pathological mechanisms of this disease are associated with the deposition of Lewy bodies (LB) composed of ASN, leading to disturbances at the molecular and subcellular levels and affecting structures such as mitochondria. Both, mitochondria and antioxidant systems are also associated with brain injury upon ischemic stroke. In the aging population the number of stroke incidents increases. Stroke in the population is expected to grow by nearly 40% over the next 20 years.
Many unexplained phenomena are implied in the aging process. This Research Topic aims to elucidate the mechanisms underlying body functioning impairment, associated with change observed in normal aging, and with the old age diseases‘ development.
It covers disorders at the molecular and functional levels in old age and may help addressing the currently unanswered questions:
-whether the brain pathologies in these individuals are associated with subtle clinical deficits,
-why various brain structures’ damage present different clinical symptoms,
-which genes and molecular factors are associated with neurodegenerative transformation,
-why Aß deposits may be found in over 80 years old individuals without showing dementia signs in normal aging.
It seems that finding the cause of pathological changes in the old age may improve health and daily functioning of older people.