Changes in the brains of patients with Alzheimer’s disease can begin decades before symptoms appear, and it only worsens as time goes on. The rate of Alzheimer's disease (AD) progression varies depending on the individual.1,2
For a detailed look at the stages of AD, click here.
Although age is the primary risk factor in Alzheimer’s disease, patients with conditions such as chronic inflammation, coronary artery disease, stroke, atrial fibrillation, hypertension, obesity, hypercholesterolemia, and type 2 diabetes face an increased risk of developing Alzheimer's disease (AD).1,3
See the underlying pathophysiological mechanisms that are thought to contribute to the development of AD here.
The first signs of Alzheimer’s disease (AD) vary but typically include memory loss, decline in cognitive functions, and changes in mood.4,5
For a detailed look at the symptoms and stages of AD, click here.
Mild cognitive impairment (MCI) due to Alzheimer’s disease (AD) involves cognitive changes that are more significant than what is typical of usual aging. Primary care physicians can perform tests to determine patients’ cognitive function and assess for potentially reversible causes of MCI.1,6,7
To discover the various reasons patients may present with MCI that are not associated with AD, click here.
Health care professionals can detect Alzheimer’s disease early by conducting annual cognitive assessments. This includes reviewing medical history, performing cognitive tests and a physical exam, conducting blood panels, and ordering imaging if needed.1,8,9
See a list of the many commonly used clinical tools to assess cognitive function here.
A cognitive test includes a thorough face-to-face examination of the patient with a focus on observing cognition. Cognitive tests also include several other elements such as a functional assessment of Basic and Instrumental Activities of Daily Living, including decision-making capacity. Some commonly used cognitive tests include the MoCA, MMSE, and the Mini-Cog.10.,11
For a list of additional clinical tools to assess cognitive function, click here.
MoCA, Montreal Cognitive Assessment; MMSE, Mini-Mental State Examination.
Alzheimer’s disease (AD) has a complex, multifactorial pathophysiology. A number of underlying mechanisms are thought to contribute to the development of AD, including the formation of Aβ plaques and tau tangles, neuroinflammation, vascular dysfunction, changes in insulin and cholesterol metabolism, and oxidative stress.4,12,13
For a deeper examination of the underlying pathophysiological mechanisms that contribute to the development of AD, start here.
Alzheimer’s disease (AD) causes neuronal dysfunction and death, affecting the parts of the brain responsible for memory and cognitive function.2
Learn about the interconnected biological processes that can contribute to AD development and progression here.
Amyloid plaques and tau tangles are the key pathological features that set Alzheimer’s disease (AD) apart from other dementias. While the buildup of Aβ is a prerequisite for the development of AD, the degree of accumulation does not directly correlate with symptoms of disease progression.2,14
To learn more about the other mechanisms contributing to the development of AD, click here.
Neuroinflammation begins as a normal response by the brain’s immune system to damage, injury, or infection. In Alzheimer’s disease (AD), this inflammation can become maladaptive, resulting in the chronic release of pro-inflammatory molecules that creates a destructive, self-amplifying cycle.14
For an in-depth look at the self-amplifying toxic cycle of neuroinflammation that occurs in the brain with AD, click here.
While there are no approved treatments yet to help reduce neuroinflammation in the brains of patients living with Alzheimer’s disease (AD), phase 3 trials are currently underway that are evaluating treatments targeting neuroinflammation pathways.15
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Currently, several classes of treatments are available to help manage Alzheimer's disease (AD) symptoms, including cholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonists. More recently, anti-amyloid treatments have been introduced as disease-modifying therapies, with the potential to slow disease progression.15
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