Alzheimer´s disease is the commonest cause of dementia affecting older people. Affects nearly 2% of the population in industrialized countries. Alzheimer´s disease is a progressive neurodegenerative disorder, pervasive in the aging population.
The risk of Alzheimer´s disease increases dramatically in individuals beyond the age of 70 and it is predicted that its incidence will increase threefold within the next 50 years.

Alzheimer´s disease results from a continuous loss of neurons, mainly in the entorhinal or paraentorhinal cortex and hippocampus. This progressive loss is preceded by a destruction of synapses (connections between neurons) and axonal damage. Neurodegeneration is accompanied by an activation of brain´s defense-cells and an abnormal increase in the number of astrocytes (cells that provide physical support to neurons and clean up debris within the brain). It results in a chronic, pro-inflammatory state. The disease starts with a mild cognitive impairment and progresses toward more severe decline and, eventually, dementia.

The neuropathological hallmarks of Alzheimer’s disease include the presence of extracellular amyloid-β peptide in the form of amyloid plaques in the brain parenchyma and neuronal loss. The mechanism associated with neuronal death by amyloid plaques is unclear but oxidative stress and glial activation has been implicated.

In recent years it has been noted that the adult brain has the ‘self-repair capacity’ to replace lost neurons in several selected regions of the central nervous system. Neural Stem cells within these neurogenic regions can proliferate and differentiate into neurons or glia, providing a reservoir for replacement of cells lost during normal cell turnover and after brain injury. Neurogenesis involves the self-renewal and proliferation of neural stem cells, as well as its differentiation into neurons and glia. Newborn neurons and glia then migrate to appropriate regions in the brain, and integrate into neuronal circuits.

Abnormalities in neural stem cells may contribute to the pathogenesis of cognitive disorders such as Alzheimer´s disease. Recent findings show that impairment of neurogenesis is sufficient to deteriorate learning and memory in rodents, hinting at a role played by abnormalities in the proliferation and differentiation of Neural Stem Cells in the pathogenesis of disorders in learning and memory such as those in Alzheimer´s disease. Synaptic dysfunction, death of mature neurons and a reduced production of new neurons from Neural Stem Cells within neurogenic niches of the Alzheimer´s disease brain may contribute to the pathogenesis of the disease.

In the early stages of Alzheimer’s disease there is a relatively discrete population of neurons affected. Thus, the disease offers a relatively discrete target for potential therapies making it an ideal target for cell replacement therapy using endogenously activated Neural stem cells. It has been suggested that mobilizing endogenous stem cells already present in the brain or transplantation of exogenous cells to replace lost cells, may be a realistic therapeutic approach.

Mesenchymal stem cell subpopulations express a variety of neuro-regulatory molecules, and promote neuronal cell survival. Neural Stem Cells transplanted at sites of nerve injury are thought to promote functional recovery by producing trophic factors that induce survival and regeneration of host neurons.

Human umbilical cord blood-derived mesenchymal stem cells are being scrutinized as a potential therapeutic tool to prevent Alzheimer’s disease. In vitro work investigations to examine the potential impact of cord blood-derived mesenchymal stem cells treatment on neuronal loss, confirmed that cord blood-derived mesenchymal stem cells reduced the hippocampal apoptosis (cellular programed death) induced by amyloid-β peptide. Moreover, in an acute Alzheimer’s disease mouse model, it has been demonstrated that markers of glial activation, oxidative stress and apoptosis levels were decreased in Alzheimer´s disease mouse brain. Interestingly, cord blood-derived mesenchymal stem cells treated Alzheimer’s disease mice demonstrated cognitive rescue with restoration of learning/memory function. These data suggest that cord blood-derived mesenchymal stem cells warrant further investigation as a potential therapeutic agent in Alzheimer´s disease.

Transplantation of Neural Stem Cells at sites of neuronal degeneration is a very promising approach for the treatment of different neurological diseases such as Alzheimer`s Disease.

Embryonic neural precursor cells provide an ideal alternative for transplantation in neurodegenerative diseases such as Alzheimer´s disease, as they can be expanded in culture, thus avoiding many of the practical obstacles that limit the application of transplanting primary neurons. It has already been shown that human Neural Stem Cells transplanted into aged rat brains can differentiate into neural cells and significantly improve the cognitive functions of animals, further pointing to Neural Stem Cells as a promising candidate for neuroreplacement therapies.

Currently, Alzheimer´s Disease therapy is only used to reduce the degree of impairment and to improve the quality of life, but the disease cannot be prevented or cured. The demonstration of active adult neurogenesis has since opened possibilities of repairing the mature Central Nervous System after degenerative neurological diseases like Alzheimer´s Disease. Ongoing research promises a bright future for the clinical application of Neural Stem Cell strategies in neuro-replacement therapy for Alzheimer´s disease patients, and may potentially reverse the progression of the disease.

There have been reports recently of the effects of Neural Stem Cells transplantation that attempt to obtain functional recovery from central nervous system damage and recent evidence suggests that Neural Stem Cells may be a suitable source for the treatment of neurological diseases such as Alzheimer´s disease or Parkinson’s disease. Nowadays, physicians are with an eye towards the development of Neural Stem Cells replacement therapies.

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