Alzheimer’s Disease (AD)

Approximately 55 million people worldwide live with dementia, of which Alzheimer’s disease accounts for about 60–70% of cases.

Alzheimer’s disease is a slow, progressive destruction of the brain that begins decades before the first sign of memory loss. The "Amyloid Cascade Hypothesis" suggests that the buildup of Amyloid Beta is the primary spark that ignites a larger fire. Once Aβ plaques reach a critical mass, they trigger a second protein called tau to malfunction and form tangles inside neurons. These tangles act like blockages in a railway, preventing nutrients from traveling through the cell. This dual attack plaques on the outside and tangles on the inside causes the brain’s immune cells (microglia) to become hyperactive and release inflammatory chemicals that damage healthy tissue. As connections between brain cells wither, the brain physically shrinks, beginning in memory centers like the hippocampus and eventually spreading to areas responsible for language, reasoning, and basic bodily functions.

Cerebral Amyloid Angiopathy (CAA)

Present in approximately 30- 40% of older adults and up to 80- 90% of patients with Alzheimer’s disease.

Cerebral Amyloid Angiopathy is a condition where Amyloid Beta deposits itself specifically within the walls of the brain’s small and medium-sized blood vessels rather than the brain tissue itself. Over time, these amyloid "bricks" replace the flexible muscular fibers of the vessel walls, making them brittle and fragile. This leads to two major problems: the vessels can become leaky, causing "microbleeds," or they can rupture entirely, leading to a major stroke. Furthermore, because the vessels are stiffened by amyloid, they cannot dilate properly to deliver more blood when the brain is working hard, leading to a "silent" lack of oxygen that contributes to cognitive decline and white matter damage.