Alzheimer’s disease (AD) constitutes a major health threat to elder people. Despite the great advances achieved regarding our knowledge of the disease, we are far to successfully treat this pathology. Molecular alterations, immune/inflammatory response, and cell death are some of the processes involved during the pathology. Moreover, AD affects the whole brain. In this regard, we must not only consider the health status of neurons, of course, but also pay attention to the status of the glial cells and additional surrounding structures, such as the blood-brain barrier (BBB). Several groups have demonstrated how the molecular alterations occurring during AD alter neurons, glial, and endothelial cells. This situation has become so relevant that different groups are currently working to unveil the blank spaces in our understanding about the co-involvement of these elements in AD. Based in our experience, we believe that this kind of approach will lead to the design and development of more comprehensive therapeutical interventions. The present chapter summarizes the relevant aspects of state of the art regarding AD, from its molecular genesis to the recent advances in neuroinflammatory modulation, including nuclear receptors (NR), such as peroxisome proliferator-activated receptors (PPARs), and the Wnt pathway involved in the AD neurodegeneration.
Part of the book: Mechanisms of Neuroinflammation
Alzheimer’s disease (AD) and Parkinson’s disease (PD) constitute the main causes of dementia worldwide and the major health threats to elderly people. Moreover, with the ageing of the global population, neurodegenerative disorders, such as AD and PD, constitute a major public health issue. Regrettably, significant advances regarding the molecular aspects of these diseases have not yet been translated into real improvements in AD/PD therapeutics. In this regard, both AD and PD are highly complex and involve critical molecular events governing the establishment and progression of each disease. Moreover, molecular alterations trigger pathophysiological cascades involving the immune/inflammatory response, oxidative stress, and mitochondrial dysfunction, among others, ultimately leading to neuronal death. Similarly, these alterations also affect glial cells and brain vasculature, which contribute directly to the progression of these disorders. Accordingly, the present paper aims to summarise the main molecular elements related to AD and PD as well as the pathophysiological implications of such alterations to improve our understanding of the cellular and molecular responses observed during neurodegeneration. We believe that providing a more comprehensive view of the pathophysiological cascade, including neurons and glial cells, might prompt researchers to widen neurodegenerative disorder research and therapeutic approaches.
Part of the book: Recent Advances in Neurodegeneration