Alzheimer's disease (AD) is the most common cause of dementia in adulthood, which is followed by cognitive impairment and behavioral deficits. Today, mesenchymal stem cell (MSC)-based therapy is a good therapeutic option to improve regenerative medicine in neurodegenerative disorders including AD. The aim of this study is to investigate the effects of the human Wharton’s jelly-derived MSCs (WJ-MSCs) on Alzheimer's rat models by studying the expression of neurotrophic factors involved in neurodegenerative diseases such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), as well as expression of apoptotic factors such as B-cell lymphoma 2 (BCL2, apoptosis inhibitor), BCL2-associated X protein (BAX, apoptosis initiator), and Caspase 3 (apoptosis executioner). Rat AD modeling was performed by intrahippocampal injection of amyloid β 1–42 (Aβ 1–42, 8 µg/kg). Animals were divided into 3 groups of 8 rat: I) control II) AD model III) MSC-treated. Behavioral tests (i.e. Passive Avoidance and Morris Water Maze) showed cognitive improvement, and amelioration of cells in the CA1 area of the hippocampus has been detected by cresyl violet (nissl) staining. Also, real-time polymerase chain reaction (RT-PCR) of the hippocampus indicated an increase in BDNF and NGF genes and a decrease in apoptosis-related genes (BCL2, BAX, and Caspase 3). Overall, WJ-MSCs improved cognitive functions in AD rat models by increasing neurotrophic factors and decreasing apoptotic factors.

Alzheimer's disease (AD) is the most common cause of dementia in adulthood, followed by cognitive and behavioral deficits. Today, mesenchymal stem cell (MSC)-based therapy is a suitable therapeutic option to improve regenerative medicine approaches against neurodegenerative disorders, including AD. This study aimed to investigate the effects of human Wharton’s jelly-derived MSCs (WJ-MSCs) on Alzheimer's rat models by evaluating the expression of neurotrophic factors involved in neurodegenerative diseases, such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), as well as the expression of apoptotic factors, such as B-cell lymphoma 2 (BCL2, an apoptosis inhibitor), BCL2-associated X protein (BAX, an apoptosis initiator), and caspase 3 (an apoptosis executioner). The AD rat modeling was performed by intrahippocampal injection of 8 µg/kg of amyloid β1-42 (Aβ1-42). The animals were divided into three groups of eight rats each: I) control; II) AD model; and III) MSC-treated model. Behavioral tests (i.e., passive avoidance and Morris water maze tests) showed cognitive improvements. Also, amelioration of cells in the CA1 area of the hippocampus was detected by cresyl violet (Nissl) staining. Besides, real-time polymerase chain reaction (RT-PCR) of the hippocampus indicated an increase in BDNF and NGF genes and a decrease in apoptosis-related genes (BCL2, BAX, and caspase 3). Overall, the WJ-MSCs improved the cognitive function in AD rat models by increasing neurotrophic factors and decreasing apoptotic factors.