Alzheimer’s Disease: Pathophysiology and Treatment
Explain the pathophysiology of Alzheimer’s disease., What are the key neurochemical and structural changes that occur in the brain and how do current pharmacological, treatments aim to slow disease progression?
Pathophysiology and Treatment of Alzheimer’s Disease
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by memory loss, cognitive decline, and behavioral changes. It is the most common cause of dementia, primarily affecting older adults. The disease results from a combination of genetic, environmental, and lifestyle factors that contribute to neuronal dysfunction and death.
Neurochemical and Structural Changes
Alzheimer’s disease is associated with two hallmark pathological features:
- Beta-amyloid plaques – These protein fragments accumulate between neurons, forming insoluble plaques that disrupt cell communication and trigger inflammatory responses, leading to neuronal damage.
- Neurofibrillary tangles (NFTs) – Abnormal accumulations of tau protein inside neurons cause tangles, disrupting the normal transport of nutrients and essential molecules within cells, ultimately leading to cell death.
Other important neurochemical changes include a significant decline in acetylcholine, a neurotransmitter essential for learning and memory. The degeneration of cholinergic neurons in the basal forebrain further exacerbates cognitive decline. Additionally, oxidative stress, chronic inflammation, and mitochondrial dysfunction contribute to disease progression.
Pharmacological Treatments
While there is no cure for Alzheimer’s, current treatments focus on slowing disease progression and managing symptoms. The main drug classes include:
- Cholinesterase Inhibitors (e.g., donepezil, rivastigmine, galantamine) – These drugs prevent the breakdown of acetylcholine, enhancing communication between neurons and temporarily improving memory and cognition.
- NMDA Receptor Antagonist (e.g., memantine) – This drug regulates glutamate activity, preventing excitotoxicity that leads to neuron damage.
- Anti-Amyloid Therapies – Newer treatments, such as monoclonal antibodies targeting beta-amyloid (e.g., aducanumab, lecanemab), aim to reduce plaque accumulation and slow disease progression.
Non-pharmacological interventions, including cognitive therapy, physical activity, and dietary modifications, also play a crucial role in managing Alzheimer’s disease. Research continues to explore novel treatments targeting tau protein and inflammation, offering hope for future advancements. APA