FREQUENTLY ASKED QUESTIONS

ABOUT ALZHEIMER’S DISEASE
ABOUT ALZHEIMER’S DISEASE
DETECTION IN PRIMARY CARE
PATHOPHYSIOLOGY
How fast does Alzheimer’s disease progress?

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.

Who is at risk for developing Alzheimer’s disease?

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.

What are the first signs of Alzheimer’s disease?

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.

How is MCI different from usual aging?

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.

How is Alzheimer’s disease detected early?

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.

What is a cognitive test?

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.

What causes Alzheimer’s disease?

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.

How does Alzheimer’s disease affect the brain?

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.

How do amyloid-β plaques and tau tangles contribute to Alzheimer’s disease?

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.

What is neuroinflammation?

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.

What can be done to reduce neuroinflammation in the brain?

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

 

Sign up for ongoing information on the latest science of AD here.

What treatment options are currently available for Alzheimer’s disease?

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

 

Sign up to receive the latest information and resources on AD here.

References
  1. Alzheimer’s Association. 2025 Alzheimer’s Disease Facts and Figures. Accessed May 22, 2025. https://www.alz.org/getmedia/ef8f48f9-ad36-48ea-87f9-b74034635c1e/alzheimers-facts-and-figures.pdf
  2. Hampel H, Hardy J, Blennow K, et al. The Amyloid-β Pathway in Alzheimer’s disease. Mol Psychiatry. 2021;26(10):5481-5503.
  3. Santiago JA, Potashkin JA. The impact of disease comorbidities in Alzheimer’s disease. Front Aging Neurosci. 2021;13:631770.
  4. Zhang J, Zhang Y, Wang J, Xia Y, Zhang J, Chen L. Recent advances in Alzheimer’s disease: mechanisms, clinical trials and new drug development strategies. Signal Transduct Target Ther. 2024;9(1):211.
  5. National Institute on Aging. What are the signs of Alzheimer’s disease? Accessed May 22, 2025. https://www.nia.nih.gov/health/alzheimers-symptoms-and-diagnosis/what-are-signs-alzheimers-disease
  6. Foster NL, Bondi MW, Das R, et al. Quality improvement in neurology: mild cognitive impairment quality measurement set. Neurology. 2019;93(16):705-713.
  7. Petersen RC, Lopez O, Armstrong MJ, et al. Practice guideline update summary: Mild cognitive impairment [RETIRED]: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology. Neurology. 2018;90(3):126-135.
  8. National Institute on Aging. How is Alzheimer’s disease diagnosed? Published 2024. Accessed May 22, 2025. https://www.nia.nih.gov/health/alzheimers-symptoms-and-diagnosis/how-alzheimers-disease-diagnosed
  9. Alzheimer’s Association. 2019 Alzheimer’s Disease Facts and Figures. Accessed May 22, 2025. https://www.alz.org/getmedia/4be8a3fe-b60d-4349-b167-8db03b16e272/alzheimers-facts-and-figures-2019-r.pdf
  10. Atri A, Dickerson BC, Clevenger C, et al. Alzheimer’s Association clinical practice guideline for the diagnostic evaluation, testing, counseling, and disclosure of suspected Alzheimer’s disease and related disorders (DETeCD-ADRD): executive summary of recommendations for primary care. Alzheimers Dement. Published online December 23, 2024.
  11. Atri A, Dickerson BC, Clevenger C, et al. The Alzheimer’s Association clinical practice guideline for the diagnostic evaluation, testing, counseling, and disclosure of suspected Alzheimer’s disease and related disorders (DETeCD-ADRD): validated clinical assessment instruments. Alzheimers Dement. 2025;21(1):e14335.
  12. DeTure MA, Dickson DW. The neuropathological diagnosis of Alzheimer’s disease. Mol Neurodegener. 2019;14(32).
  13. Calabrò M, Rinaldi C, Santoro G, Crisafulli C. The biological pathways of Alzheimer disease: a review. AIMS Neurosci. 2020;8(1):86-132.
  14. Leng F, Edison P. Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here? Nat Rev Neurol. 2021;17(3):157-172.
  15. Cummings J, Zhou Y, Lee G, Zhong K, Fonseca J, Cheng F. Alzheimer’s disease drug development pipeline: 2024. Alzheimer’s Dement (N Y). 2024;10(2).
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