Mitochondrial Dysfunction in Alzheimer’s Disease: A Biomarker of the Future?

Abstract

Alzheimer’s disease (AD) is the most common cause of dementia worldwide and is characterised pathologically by the accumulation of amyloid beta and tau protein aggregates. Currently, there are no approved disease modifying therapies for clearance of either of these proteins from the brain of people with AD. As well as abnormalities in protein aggregation, other pathological changes are seen in this condition. The function of mitochondria in both the nervous system and rest of the body is altered early in this disease, and both amyloid and tau have detrimental effects on mitochondrial function. In this review article, we describe how the function and structure of mitochondria change in AD. This review summarises current imaging techniques that use surrogate markers of mitochondrial function in both research and clinical practice, but also how mitochondrial functions such as ATP production, calcium homeostasis, mitophagy and reactive oxygen species production are affected in AD mitochondria. The evidence reviewed suggests that the measurement of mitochondrial function may be developed into a future biomarker for early AD. Further work with larger cohorts of patients is needed before mitochondrial functional biomarkers are ready for clinical use.

Mitochondrial Dysfunction as a Driver of Cognitive Impairment in Alzheimer’s Disease

“…Besides, availability of information related to mitochondrial proteomic has opened the door that uncovers various aspects of this energy associated organelle, which further adds on the understanding of mitochondrial dysfunction in AD [28]. Thus, sustaining mitochondrial function therapeutically may forestall neurodegeneration and loss of cognition in AD [30,31]. Given the likely importance of mitochondrial dysfunction in AD pathogenesis, this work summarizes the molecular mechanisms for mitochondrial dysfunction contributing to cognitive impairment in AD.…”

‘The awesome power of yeast’ in Alzheimer’s disease research

“…Mitochondrial dysfunction and impaired mitophagy are common features of AD 28 . The fact that mammalian cells are not able to survive with defective mitochondria makes it impossible for studies involving investigations on mitochondrial health.…”

Volume 42 Number 3

“…(n = 56/87, 64.4%) 28 and 2016 (n = 386/521, 74.0%) 29 . The annualised rate of ESBL-producing E. coli circulating New Zealand is has also increased nation-wide, particularly between 2008 and 2013 (Figure 4).…”

“…The presence of healthy carriers of NTHi indicates that a complete eradication of NTHi is not necessary to prevent infection. Furthermore, higher NTHi pharyngeal carriage loads are correlated with an increased susceptibility to otitis media in vivo [27][28][29][30] and an increased severity of airway inflammation, exacerbations, and daily symptoms in chronic obstructive pulmonary disease 31,32 . Thus, even small reductions in NTHi carriage might have beneficial clinical outcomes.…”