Abstract
Alzheimer’s disease and cancer are known to be very serious disorders that can cause death especially in the elderly. The prevalence of cancer is dramatically increased with age, correspondingly, Alzheimer’s disease (AD) is an age-dependent neurodegenerative disorder. Cancer is defined as a disease in which a collection of abnormal cells divides uncontrollably by ignoring the normal principles of cell division. There is known to be more than 200 types of cancers and its two main characteristics are uncontrolled growth of the cells in the human body and the ability of these cells to migrate from the original site and spread to distant sites. On the other hand, Alzheimer’s disease is a progressive neurodegenerative disorder that is …show more content…
It processed that the mutations in the genes encoding Amyloid Precursor Protein (APP), Presenilin I (PSI) and Presenilin II (PSII) which are linked to AD suggested that Aβ peptide is the major initiator of the development of AD. It stated that the deposition of β-amyloid (Aβ) was the initial pathological event in Alzheimer’s disease resulting to the formation of neurofibrillary tangles (NFTs) and senile plaques (SPs), neuronal cell death and ultimately dementia (Maloney, 2015). Scientists assessed this hypothesis in 1989 by expressing the Aβ peptide in a cell line called PC-12cells that could be stimulated to differentiate to neurons when cultivated in the presence of nerve growth factor (NGF) (Yankner et al. 1989). The researchers found that the PC-12 cells grew normally while expressing the Aβ peptide, up until they were treated with nerve growth factor and stimulated to differentiate into neurons, at which time they began to degenerate and die. Furthermore, treating cultured neurons with cell growth medium from the Aβ-expressing PC-12 cells also caused degeneration and cell death (Yankner et al. 1989). This degeneration could be blocked to some extent if the cell growth medium was initially treated with an antibody against Aβ (Yankner et al. 1989). These results suggested that the Aβ peptide is an active and soluble agent causing degeneration in …show more content…
Many of these failed trials enrolled many patients in the late‐mild or moderate stages of Alzheimer’s Disease, while other trials conducted in very mild or mild Alzheimer’s Disease delivered suggestive evidence of clinical advantage. Alzheimer’s Disease trials done preceding compulsory amyloid‐PET imaging turned out to have up to 25% of subjects that were amyloid‐negative
A theory that Alzheimer’s disease is fundamentally due to loss of presenilin (PSI and PSII) function were put forward Alzheimer’s Disease causing (PSI and PSII) mutations may indeed act through slight loss of function of this protease, but these heterozygous mutations do not generate clinically detectable loss of (PSI and PSII) function (e.g., Notch phenotypes), and organismal development and function are normal until the carriers develop typical AD symptoms in mid‐life, heralded by elevated Aβ42/43 to Aβ40 ratios. Moreover, 99.9% of all Alzheimer’s Disease patients have wild‐type
Alzheimer’s disease and cancer are known to be very serious disorders that can cause death especially in the elderly. The prevalence of cancer is dramatically increased with age, correspondingly, Alzheimer’s disease (AD) is an age-dependent neurodegenerative disorder. Cancer is defined as a disease in which a collection of abnormal cells divides uncontrollably by ignoring the normal principles of cell division. There is known to be more than 200 types of cancers and its two main characteristics are uncontrolled growth of the cells in the human body and the ability of these cells to migrate from the original site and spread to distant sites. On the other hand, Alzheimer’s disease is a progressive neurodegenerative disorder that is …show more content…
It processed that the mutations in the genes encoding Amyloid Precursor Protein (APP), Presenilin I (PSI) and Presenilin II (PSII) which are linked to AD suggested that Aβ peptide is the major initiator of the development of AD. It stated that the deposition of β-amyloid (Aβ) was the initial pathological event in Alzheimer’s disease resulting to the formation of neurofibrillary tangles (NFTs) and senile plaques (SPs), neuronal cell death and ultimately dementia (Maloney, 2015). Scientists assessed this hypothesis in 1989 by expressing the Aβ peptide in a cell line called PC-12cells that could be stimulated to differentiate to neurons when cultivated in the presence of nerve growth factor (NGF) (Yankner et al. 1989). The researchers found that the PC-12 cells grew normally while expressing the Aβ peptide, up until they were treated with nerve growth factor and stimulated to differentiate into neurons, at which time they began to degenerate and die. Furthermore, treating cultured neurons with cell growth medium from the Aβ-expressing PC-12 cells also caused degeneration and cell death (Yankner et al. 1989). This degeneration could be blocked to some extent if the cell growth medium was initially treated with an antibody against Aβ (Yankner et al. 1989). These results suggested that the Aβ peptide is an active and soluble agent causing degeneration in …show more content…
Many of these failed trials enrolled many patients in the late‐mild or moderate stages of Alzheimer’s Disease, while other trials conducted in very mild or mild Alzheimer’s Disease delivered suggestive evidence of clinical advantage. Alzheimer’s Disease trials done preceding compulsory amyloid‐PET imaging turned out to have up to 25% of subjects that were amyloid‐negative
A theory that Alzheimer’s disease is fundamentally due to loss of presenilin (PSI and PSII) function were put forward Alzheimer’s Disease causing (PSI and PSII) mutations may indeed act through slight loss of function of this protease, but these heterozygous mutations do not generate clinically detectable loss of (PSI and PSII) function (e.g., Notch phenotypes), and organismal development and function are normal until the carriers develop typical AD symptoms in mid‐life, heralded by elevated Aβ42/43 to Aβ40 ratios. Moreover, 99.9% of all Alzheimer’s Disease patients have wild‐type