Huntington's disease (HD) is a progressive, fatal neurodegenerative disease caused by expanded polyglutamine repeats in the HD gene. HD is characterized by chorea, seizures, involuntary movements, dystonia, cognitive decline, intellectual impairment and emotional disturbances. Research into mutant huntingtin (Htt) and mitochondria has found that mutant Htt interacts with the mitochondrial protein dynamin-related protein 1 (Drp1), enhances GTPase Drp1 enzymatic activity, and causes excessive mitochondrial fragmentation and abnormal distribution, leading to defective axonal transport of mitochondria and selective synaptic degeneration. This article summarizes latest developments in HD research and focuses on the role of abnormal mitochondrial dynamics and defective axonal transport in HD neurons. This article also discusses the therapeutic strategies that decrease mitochondrial fragmentation and neuronal damage in HD. (C) 2011 Elsevier B.V. All rights reserved.

Mitochondria play a large role in neuronal function by constantly providing energy, particularly at synapses. Recent studies suggest that amyloid beta (A beta) and phosphorylated tau interact with the mitochondrial fission protein, dynamin-related protein 1 (Drp1), causing excessive fragmentation of mitochondria and leading to abnormal mitochondrial dynamics and synaptic degeneration in Alzheimer's disease (AD) neurons. Recent research also revealed A beta-induced and phosphorylated tau-induced changes in mitochondria, particularly affecting mitochondrial shape, size, distribution and axonal transport in AD neurons. These changes affect mitochondrial health and, in turn, could affect synaptic function and neuronal damage and ultimately leading to memory loss and cognitive impairment in patients with AD. This article highlights recent findings in the role of Drp1 in AD pathogenesis. This article also highlights Drp1 and its relationships to glycogen synthase kinase 3, cyclin-dependent kinase 5, p53, and microRNAs in AD pathogenesis. (C) 2015 Elsevier B.V. All rights reserved.

Recently researchers proposed the term 'Type-3-Diabetes' for Alzheimer's disease (ad) because of the shared molecular and cellular features among Type-1-Diabetes, Type-2-Diabetes and insulin resistance associated with memory deficits and cognitive decline in elderly individuals. Recent clinical and basic studies on patients with diabetes and AD revealed previously unreported cellular and pathological among diabetes, insulin resistance and AD. These studies are also strengthened by various basic biological studies that decipher the effects of insulin in the pathology of AD through cellular and molecular mechanisms. For instance, insulin is involved in the activation of glycogen synthase kinase 313, which in turn causes phosphorylation of tau, which involved in the formation of neurofibrillary tangles. Interestingly, insulin also plays a crucial role in the formation amyloid plaques. In this review, we discussed significant shared mechanisms between AD and diabetes and we also provided therapeutic avenues for diabetes and AD. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondria) Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases-edited by P. Hemachandra Reddy. (C) 2016 Elsevier B.V. All rights reserved.

The purpose of this review article is to understand the current literature on obesity, diabetes and therapeutic avenues across the world. Diabetes is a chronic lifestyle condition that affects millions of people worldwide and it is a major health concern in our society. Diabetes and obesity are associated with various conditions, including non modifiable and modifiable risk factors. Early detectable markers are not well established to detect pre-diabetes and as a result, it becomes diabetes. Several published epidemiological studies were assessed and the findings were summarized. Resources from published studies were used to identify criteria used for pre-diabetes, the role of diet in pre-diabetics and potential risks and characteristics associated with pre-diabetes. Preventive strategies are needed to combat diabetes. Individuals diagnosed with pre-diabetes need detailed education, need to fully understand the risk factors and have the ability to manage diabetes. Interventions exist that include chronic disease self-management programs, lifestyle interventions and pharmacological strategies. Obesity plays a large role in causing pre-diabetes and diabetes. Critical analysis of existing epidemiological research data suggests that additional research is needed to determine the efficacy of interventions. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases edited by P. Hemachandra Reddy. (C) 2017 Elsevier B.V. All rights reserved.

Alzheimer's disease (AD) is an age-related progressive neurodegenerative disease affecting thousands of people in the world and effective treatment is still not available. Over two decades of intense research using AD postmortem brains, transgenic mouse and cell models of amyloid precursor protein and tau revealed that amyloid beta (A beta) and hyperphosphorylated tau are synergistically involved in triggering disease progression. Accumulating evidence also revealed that aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction initiate and contributes to the development and progression of the disease. The purpose of this article is to summarize the latest progress in aging and AD, with a special emphasis on the mitochondria, oxidative DNA damage including methods of its measurement. It also discusses the therapeutic approaches against oxidative DNA damage and treatment strategies in AD. (C) 2011 Elsevier B.V. All rights reserved.

Stroke is the second leading cause of death in the world. Stroke occurs when blood flow stops, and that stoppage results in reduced oxygen supply to neurons in the brain. The occurrence of stroke increases with age, but anyone at any age can suffer from stroke. Recent research has implicated multiple cellular changes in stroke patients, including oxidative stress and mitochondrial dysfunction, inflammatory responses, and changes in mRNA and proteins. Recent research has also revealed that stroke is associated with modifiable and non-modifiable risk factors. Stroke can be controlled by modifiable risk factors, including diet, cardiovascular, hypertension, smoking, diabetes, obesity, metabolic syndrome, depression and traumatic brain injury. Stroke is the major risk factor for vascular dementia (VaD) and Alzheimer's disease (AD). The purpose of this article is to review the latest developments in research efforts directed at identifying 1) latest developments in identifying biomarkers in peripheral and central nervous system tissues, 2) changes in microRNAs (miRNAs) in patients with stroke, 3) miRNA profile and function in animal brain, and 4) protein biomarkers in ischemic stroke. This article also reviews research investigating circulatory miRNAs as peripheral biomarkers of stroke. (C) 2016 Elsevier B.V. All rights reserved.