Alzheimer’s disease (AD) is the leading cause of dementia in elderly people. Amyloid beta (Aβ) deposits and neurofibrillary tangles are the major pathological features in an Alzheimer’s brain. These proteins are highly expressed in nerve cells and found in most tissues. Tau primarily provides stabilization to microtubules in the part of axons and dendrites. However, tau in a pathological state becomes hyperphosphorylated, causing tau dysfunction and leading to synaptic impairment and degeneration of neurons. This article presents a summary of the role of tau, phosphorylated tau (p-tau) in AD, and other tauopathies. Tauopathies, including Pick’s disease, frontotemporal dementia, corticobasal degeneration, Alzheimer’s disease, argyrophilic grain disease, progressive supranuclear palsy, and Huntington’s disease, are the result of misprocessing and accumulation of tau within the neuronal and glial cells. This article also focuses on current research on the post-translational modifications and genetics of tau, tau pathology, the role of tau in tauopathies and the development of new drugs targeting p-tau, and the therapeutics for treating and possibly preventing tauopathies.

Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in elderly individuals. AD occurs in two forms, early onset familial and late-onset sporadic; genetic mutations in PS1, PS2, and APP genes cause early onset familial AD, and a combination of lifestyle, environment and genetic factors causes the late-onset sporadic form of the disease. However, accelerated disease progression is noticed in patients with familial AD. Disease-causing pathological changes are synaptic damage, and mitochondrial structural and functional changes, in addition to increased production and accumulation of phosphorylated tau (p-tau), and amyloid beta (Aβ) in the affected brain regions in AD patients. Aβ is a peptide derived from amyloid precursor protein (APP) by proteolytic cleavage of beta and gamma secretases. APP is a glycoprotein that plays a significant role in maintaining neuronal homeostasis like signaling, neuronal development, and intracellular transport. Aβ is reported to have both protective and toxic effects in neurons. The purpose of our article is to summarize recent developments of Aβ and its association with synapses, mitochondria, microglia, astrocytes, and its interaction with p-tau. Our article also covers the therapeutic strategies that reduce Aβ toxicities in disease progression and discusses the reasons for the failures of Aβ therapeutics.

With increasing aging, dementia is a growing public health concern globally. Patients with dementia have multiple psychological and behavioral changes, including depression, anxiety, inappropriate behavior, paranoia, agitation, and hallucinations. The major types of dementia are Alzheimer’s disease (AD), vascular dementia (VCID), Lewy body dementia (LBD), frontotemporal dementia (FTD), and mixed dementia (MiAD). Among these, AD is the most common form of dementia in the elderly population. In the last three decades, tremendous progress has been made in understanding AD’s biology and disease progression, particularly its molecular basis, biomarker development, and drug discovery. Multiple cellular changes have been implicated in the progression of AD, including amyloid beta, phosphorylated tau, synaptic damage, mitochondrial dysfunction, deregulated microRNAs, inflammatory changes, hormonal deregulation, and others; based on these changes, therapeutic strategies have been developed, which are currently being tested in animal models and human clinical trials. The purpose of our article is to highlight recent therapeutic strategies’ developments, critically discuss current strategies’ failures, and propose new strategies to combat this devasting mental illness.

Cancer is a public health concern and causes more than 8 million deaths annually. Cancer triggers include population growth, aging, and variations in the prevalence and distribution of the critical risk factors for cancer. Multiple hallmarks are involved in cancer, including cell proliferation, evading growth suppressors, activating invasion and metastasis, resisting cell death, enabling replicative immortality, reprogramming energy metabolism, and evading immune destruction. Both cancer and dementia are age-related and potentially lethal, impacting survival. With increasing aging populations, cancer and dementia cause a burden on patients, family members, the health care system, and informal/formal caregivers. In the current article, we highlight cancer prevalence with a focus on different ethnic groups, ages, and genders. Our article covers risk factors and genetic causes associated with cancer and types of cancers and comorbidities. We extensively cover the impact of cancer in Hispanics in comparison to that in other ethnic groups. We also discuss the status of caregivers with cancer patients and urgent needs from the state and federal support for caregivers.

Diabetes is an age-related chronic health condition and a major public health concern. Diabetes is one of the significant causes of morbidity and mortality and a major contributing factor to dementia. Recent research reveals that Hispanic Americans are at an increased risk of chronic conditions such as diabetes, dementia, and obesity. Recent research also revealed that diabetes develops at least ten years earlier in Hispanics and Latinos than in neighboring non-Hispanic whites. Furthermore, the management of diabetes and providing necessary/timely support is a challenging task for healthcare professionals. Caregiver support is an emerging area of research for people with diabetes, mainly family caregiver support work for Hispanic and Native Americans. Our article discusses several aspects of diabetes, factors associated with diabetes among Hispanics, its management, and how caregivers can support individuals with diabetes.