The Biological Basis of Alzheimer’s (Beta-Amyloid, Tau)

First described in 1906 by Alois Alzheimer, Alzheimer’s disease is biologically defined by two interacting protein pathologies: extracellular beta-amyloid plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau. In 1984, George Glenner and colleagues identified the amyloid-β peptide as the principal component of plaques, and in 1991 John Hardy formulated the amyloid cascade hypothesis, proposing that abnormal accumulation of amyloid-β initiates synaptic dysfunction, neuroinflammation, and downstream tau pathology; meanwhile, foundational work by Michel Goedert in the late 1980s and 1990s clarified how tau, a microtubule-associated protein, becomes misfolded and aggregated into paired helical filaments that disrupt neuronal transport and lead to cell death. Together these processes progressively damage hippocampal and cortical networks responsible for memory, reasoning, and identity.

From a Christian perspective grounded in the Bible, such research reflects the Genesis mandate to steward creation (Genesis 1:28) and embodies Christ’s call to compassionate care for the vulnerable (Matthew 25:36), while theologians such as Augustine of Hippo emphasised that human frailty, though a mark of the Fall (Romans 5:12), does not erase the imago Dei, the enduring dignity of persons even amid cognitive decline.

Understanding beta-amyloid and tau therefore serves not only scientific progress but personal wellbeing, by fostering earlier diagnosis, risk reduction, and targeted therapies. Such an understanding may also serve societal health, by guiding public policy, reducing caregiver burden, and cultivating communities that respond to neurodegeneration with informed hope, ethical responsibility, and sacrificial love.