Contents


**Chapter 7 105** An Examination of Factors Influencing Equitable Access to Dementia Care and Support Programs among Migrants and Refugees Living with Dementia: A Literature Review *by Winnie Sun, Srija Biswas, Michelle Dacanay and Ping Zou*

Preface

It is fair to say that no brain disease occupies more research study today than Alzheimer's disease (AD). Among the many excellent reasons for this circumstance are the bleak prognosis and relentless progression; large cohorts of baby boomers entering an age of greatly increased cognitive risk; spectacular advances in medical care that have prolonged lifespan; and ever-mounting risk with age. Moreover, there is perhaps no dearer feature than self-awareness and the memory of self across

Often unattributed in propelling interest in AD is the success of the research enterprise that has advanced the understanding of the brain. From Hodgkin and Huxley's characterization of the action potential less than 70 years ago, neuroscience has identified nearly all brain neurotransmitters, resolved the structure of the major ion channels, and stands poised to decipher the operations of hundreds of thousands of neurons in joint activity. The product of the scientific method of these successes have instilled a confidence that disease causes will ultimately succumb to the persistence of research, and that the accumulation of data from appropriately designed experiments will blossom into therapies that will arrest and perhaps even reverse AD. Such confidence is being tested, however, and may be prolonged by the very strategies that repeat the premises of the past research methods that have so successfully propelled other aspects of neuroscientific

Despite the decades of intense research and a rising wave of elderly people, AD remains poorly understood, an enigma amid a tide of neuroscientific advance. Identified more than a century ago, AD is characterized by a constellation of cognitive dysfunctions, the earliest and most prominent being that of impaired recollection. In its many decades of investigation, numerous theories have sought to unify AD's disparate symptoms within a common causal frame. Current readings list some 13 influential hypotheses, the most widely invoked involving the biomarkers, β-amyloid plaques, and neurofibrillary tangles, identified by Alois Alzheimer more than 100 years ago. Other frequently cited causes include dysfunctional energy resourcing, with evidence pointing toward either glycolytic or electron transport

The mystery of AD's origin is compounded by the genetic observations intended to provide improved predictive diagnosis for a swelling demographic sector. Its set of risk alleles is large by non-cognitive disease standards, and new alleles are regularly being added. The current membership is highly diverse, with some alleles affecting the early onset phase, such as the presenilin genes, the late-phase β-amyloid protein, lipidogenesis genes, and even cytoskeletal and immune genes, among a growing set. Most alleles display small phenotypic effects that are non-Mendelian with low penetrance and that are of a quantitative rather than a qualitative nature. Overall, the relatively small effects of individual alleles and the large field of membership obscure rather than enlighten, offering meager

time, all of which are taken as the disease marks its course.

research.

stages.
