This project delves into the neurobiological mechanisms underlying memory formation, retention, and the pathological forgetting associated with Alzheimer's disease (AD). Memory formation involves encoding, storage, and retrieval processes facilitated by synaptic plasticity, which allows neurons to strengthen or weaken their connections based on activity. In Alzheimer's disease, this process is disrupted, leading to significant memory loss and cognitive decline. Alzheimer's is characterized by the accumulation of beta-amyloid plaques and neurofibrillary tangles (NFTs) in the brain, which disrupt neural communication and lead to cell death. The hippocampus, crucial for memory, is particularly affected, leading to early symptoms like memory loss and confusion. As the disease progresses, it spreads to other brain regions, further impairing cognitive and bodily functions. While there is no cure for Alzheimer's, treatments like cholinesterase inhibitors can manage symptoms in the early stages. Physical exercise, particularly aerobic and resistance training, has shown potential in improving cognitive function and delaying the onset of symptoms. Ongoing research focuses on early diagnosis and novel therapies, including drug trials aimed at reducing tau aggregation and beta-amyloid plaques, offering hope for future advancements in Alzheimer's treatment.
Healthy brain on left and Alzheimer’s disease severe brain on right. (Figure representation created by the authors)
Protein Tau assembles on healthy microtubules on top and misfolded protein. (Figure representation created by the authors)
Cancer is fundamentally a disease of gene expression and regulation. Research has focused on the pathways around promoting cell division (e.g. Ras and the promotion of excessive cell division) or the pathways around inhibiting cell growth. Multiple gene mutations are typically required before the development of cancer.
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