Alzheimer's disease (AD), the most common cause of dementia, causes progressive memory loss, impaired intellect, loss of coordination, and an inexorable decline in the ability to perform daily tasks. The exact cause of the condition is not known and there is no cure, but some therapies may help ease symptoms.
Biomarkers: Amyloid Plaque
Pictured is a light micrograph of brain tissue showing amyloid plaque, a characteristic biomarker of AD. The fragmented protein, beta-amyloid, accumulates between neurons and can begin forming as much as 10 to 20 years prior to symptom onset. Amyloid has been the focus of most Alzheimer’s therapy research; however another misfolded protein is beginning to share the spotlight.
Biomarkers: Neurofibrillary Tangles
Pictured is a colored transmission electron micrograph of a neurofibrillary tangle in a neuron from the brain of a patient with AD. The tangle (green) lies in the cytoplasm of the cell and consists of abnormal aggregates of the protein tau. It is not known precisely how the tangles are formed, or their impact on neuron function, but they are seen in a range of neurologic disorders. Recent research suggests that tau accumulation may be a more suitable marker of transition to mild Alzheimer’s from the pre-symptomatic stage.
1. Brier MR, Gordon B, Friedrichsen K, et al. Tau and Aβ imaging, CSF measures, and cognition in Alzheimer's disease. Sci Transl Med. 2016;8(338):338ra66.
You can skip this ad in 3 seconds.
Biomarkers: Brain Atrophy
Over time, the degeneration of synaptic connections causes neuronal injury and death. This widespread neuronal death eventually causes atrophy of key brain regions, namely the hippocampus and temporal lobe, although widespread cerebral atrophy is seen in advanced cases of the disease.
AD is typically only definitively diagnosed posthumously; however researchers are now focusing on 23 areas of diagnostics to help diagnose and initiate treatment earlier. CSF biomarkers, imaging, and standardized clinical tests of cognition can be utilized alone or together to determine AD risk. Researchers also continue to explore the utility of genetic testing, insulin resistance, and assessment of sensory and motor changes as markers of the disease.
Treatment and Prevention
While current therapies can only quell AD symptoms, there are a growing number of pharmaceutical and alternative treatment options to address the different symptoms and side effects of AD. Cognitive deficits are typically treated with cholinesterase inhibitors or memantine, which help to prevent the breakdown of acetylcholine and regulate glutamate activity. Non-drug approaches are favored to address changes in patient behavior, although antidepressants and antipsychotics may be utilized. In pre-symptomatic people, staying mentally and physically active may have beneficial effects on brain health. Moderate exercise, reading, writing, and engaging in other active-thought activities, as well as regular socialization may help exert a protective effect on the brain.
Alzheimer disease is an irreversible, progressive brain disease that slowly destroys memory and thinking skills. It is the sixth leading cause of death in the US, where an estimated 5.4 million Americans are living with the disease. In most people with Alzheimer’s, symptoms first appear after age 65, although an estimated 5% of patients will experience early-onset of the disease before age 65.