David F. Tang-Wai, MDCM, FRCPC, Assistant Professor, University of Toronto; Division of Neurology, University Health Network Memory Clinic, Toronto Western Hospital, Toronto, ON.

Alzheimer’s disease is the most common cause of dementia among older adults. After a century of research, there have been significant scientific advances in the understanding of this disorder. Over the past 15 years, treatment for Alzheimer’s disease exists but it is symptomatic and its effects are modest at best. Currently, newer disease-modifying treatments are being investigated that have the potential of slowing the progression of the disease.
Key words: Alzheimer’s disease, disease-modifying agents, amyloid, tau, neuroprotection.

Elliott M. Kanner, MD, PhD, Department of Ophthalmology, Edward S. Harkness Eye Institute, Columbia University College of Physicians and Surgeons, New York, NY, USA.
James C. Tsai, MD, Associate Professor and Director, Glaucoma Division, Department of Ophthalmology, Edward S. Harkness Eye Institute, Columbia University College of Physicians and Surgeons, New York, NY, USA.

Glaucoma is a sight-threatening, progressive optic neuropathy whose incidence increases with age. Currently, the only proven treatment for glaucoma is the reduction of intraocular pressure (IOP). As medical treatment has become safer and diagnostic modalities have become more sensitive, it has become possible to detect and treat glaucoma earlier. This means that with more aggressive screening and treatment, a common cause of irreversible blindness can be prevented. As more patients are treated earlier, it is important not only for ophthalmologists but also for primary care physicians to be aware of the barriers to adherence and possible interactions and side effects of glaucoma medications. Parallels between glaucoma and other neurodegenerative disease are stimulating new approaches to therapy beyond IOP control, targeted directly at the prevention of axonal loss.
Key words: glaucoma, intraocular pressure, medications, neuroprotection, retinal ganglion cell.