This book focuses on the public policy and political dimensions of Alzheimer’s Disease and other dementias (AD/D) in the United States, with coverage of the global dimensions and relevant examples from other countries. Starting off with a discussion on the characteristics of AD/D and competing theories of their causes, their human and financial costs, and the increasing burden they place on all societies as populations age, the book examines in detail the range of policy issues they raise. These include funding policies, payment policy and regulatory functions, long-term services and support (LTCS), public health and prevention policies. The book analyses the big business surrounding AD/D and shows that the strong public fear of developing dementia heightens the likelihood of exploitation of vulnerable people looking for a technological fix. It examines both informal and formal caregivers and the heavy burden placed on families, primarily women, and recent policy attempts to strengthen LTCS. It also examines the latest evidence of potential risk-reduction and prevention strategies and the difficult issues surrounding advance directives, assisted suicide, and definitions of death that increasingly face policy makers. It concludes by analyzing the policy implications on possible technological scenarios.

Subjective cognitive decline (SCD) with self-reported concerns and mild cognitive impairment (MCI) are well-established to be at increased risk of developing Alzheimer’s disease (AD) dementia and a clinical continuum of dementia progression as a spectrum of AD. AD may develop from SCD to MCI (early MCI and late MCI) and eventually to AD. Nevertheless, until recently little was known about their pathophysiology associated with cognitive-behavioral syndrome. Although for researchers, scientists and clinicians, the pathophysiology of AD spectrum is an intriguing issue, delineating it in a clear way is far from easy. Taken together, in-depth understanding of neuroimaging-based pathology behind cognitive impairments across AD spectrum may help to develop new strategy for the early diagnosis and treatment of AD. Neuroimaging has been thought to potentially reveal the pathological mechanisms of AD progression. Individuals across AD spectrum are often associated with anatomical and functional brain alterations and cognitive impairment, most of the pathophysiology will focus primarily on the brain. To investigate brain structures and functions associated with cognition, neuroimaging will be the most appropriate tool.

Emerging data suggest a link between Alzheimer’s disease (AD) and epilepsy. AD and other dementias pose increased risk for seizures, with seizure incidence in AD up to ten times greater than in age-matched controls. Mouse models of AD also demonstrate seizures and abnormal spikes or sharp wave discharges (“interictal epileptiform discharges” [IEDs]) on electroencephalography (EEG). Seizures and IEDs may underlie fluctuating cognitive abilities in AD, with the impact of antiseizure medication (ASM) requiring further investigation. Many epilepsy patients have memory and other cognitive deficits, due to multiple factors. Most adult-onset epilepsy occurs in people =60 years of age, and epilepsy patients are at increased risk of developing dementia. Hyperphosphorylated tau and amyloid deposits were found in resected temporal lobe tissue of epilepsy patients, similar to AD, and increased total and phosphorylated tau levels in the cerebrospinal fluid may predict the onset of AD and other dementias. The mechanisms underlying the associations between AD, epilepsy, tau deposition, and beta amyloid plaques, and their relationships to clinical features, are unknown. Some epilepsy patients develop dementia, and some AD patients develop seizures, while others do not. Analyses of resected tissue in epilepsy patients also suggest variable amyloid and tau deposition across patients and studies. Who is at risk? What does shared pathology indicate regarding disease development, progression, and treatment? Better understanding of the associations between epilepsy and dementia with respect to epidemiology, pathophysiology, genetics, clinical presentations, and treatment approaches based on animal models and human studies is needed to optimize patient care. Insight into the relationship between epilepsy and AD requires various approaches, including tissue analysis, imaging, genetic techniques, cognitive testing, and electroencephalography in animals and humans. We welcome manuscripts that span these approaches, including original research articles, brief research articles, clinical trials, case reports, reviews, systematic reviews, mini-reviews, methods articles, hypothesis and theory articles, perspectives, and opinions. Themes may include: • Diagnosis (e.g., seizure or interictal discharge detection in dementia patients, distinguishing comorbid dementia from epilepsy-related cognitive dysfunction) • Epidemiology (e.g., incidence and prevalence of comorbid AD and epilepsy, occurrence of epilepsy in other dementias, seizure types, age or stage of onset) • Genetic risk factors • Pathophysiology underlying seizure generation in AD and cognitive decline in epilepsy • Treatment approaches (e.g., effects of ASMs on cognitive decline, impact of disease modifying AD treatments on seizures, neurostimulation) • What can be learned from other disorders in which cognitive deficits and seizures are common (i.e., traumatic brain injury)

February issue includes Appendix entitled Directory of United States Government periodicals and subscription publications; September issue includes List of depository libraries; June and December issues include semiannual index