Alzheimer's disease (AD) is the most common form of dementia whose incidence is increasing at an alarming rate worldwide. There are many factors contributing to this scenario including the aging of the population, unhealthy lifestyle habits and lack of effective treatments.
The extensive research undertaken in the last decades has unrevealed several mechanisms underlying AD pathophysiology. However, concerning sporadic AD, which represents more than 99% of all cases, the cause(s) has(have) been surrounded by intense controversy. There is an urgent need to disclose the precipitating mechanisms to develop more efficient strategies to fight this devastating disease.
Many lines of evidence demonstrate that deficits in energy metabolism, involving changes in cerebral blood flow, glucose metabolism and mitochondria homeostasis, play a crucial and early role in the degenerative cascade that occurs in AD. This mini‐symposium is devoted to provide a greater insight into the role played by these factors in this disease and how they can be detected and prevented or minimized.
The paper by Love and Miners 1 discusses how functional and structural anomalies of the cerebral vasculature contribute to hypoperfusion and energy deficit in AD and the implications of the use of hypertensive drugs. This topic is further developed in the paper by de la Torre 2, where interventions aimed to enhance cerebral perfusion and their possible efficacy in AD are discussed. Cardoso and colleagues 3 give an updated view of the role of mitochondrial anomalies in AD and discuss several pharmacological and lifestyle interventions that may help preserve mitochondrial homeostasis. In the same line, the paper by Bernardo and colleagues 4 highlight the beneficial aspects of physical exercise in brain fitness and cognitive health, putting the focus on mitochondria. Finally, the paper by Shokouhi and colleagues 5 discusses critical barriers in conventional longitudinal positron emission tomography (PET) imaging that may be particularly relevant for early AD studies.
References
- 1. Love S, Miners JS (2016) Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease. Brain Pathol 26:607–617. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. dela Torre JC (2016) Cerebral perfusion enhancing interventions: a new strategy for the prevention of Alzheimer Dementia. Brain Pathol 26:618–631. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Cardoso S, Carvalho C, Correia S, Seica RM, Moriera PI (2016) Alzheimer's Disease: From Mitochondrial Perturbations to Mitochondrial Medicine. Brain Pathol 26:632–647. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Bernardo TC, Marques-Aleixo I, Beleza J, Oliveira PJ, Ascensao A, Magalhaes J (2016) Physical Exercise and Brain Mitochondrial Fitness: The Possible Role Against Alzheimer's Disease. Brain Pathol 26:648–663. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5. Shokouhi S, Campbell D, Brill AB, Gwirtsman HE (2016) The Alzheimer's Disease Neuroimaging initiative. Brain Pathol 26:664–671. [DOI] [PMC free article] [PubMed] [Google Scholar]
