Alzheimer’s disease is the main cause of dementia, contributing to an estimated 60 to 70 percent of all cases worldwide. It is one of several diseases that damage the brain and progressively impair memory, thinking, and the ability to carry out everyday tasks. But dementia is rarely simple. The second and third most common types, vascular dementia and Lewy body dementia, each involve different mechanisms, and many people have more than one type at the same time.
How Alzheimer’s Disease Damages the Brain
Alzheimer’s involves two abnormal proteins that gradually destroy brain cells. The first, called amyloid, normally floats harmlessly in the brain. In Alzheimer’s, amyloid fragments clump together into small, highly toxic clusters called oligomers. These clusters interfere with the way brain cells communicate with each other and eventually kill them.
The second protein, called tau, has a useful job in healthy brains: it stabilizes the internal scaffolding that cells rely on to transport nutrients and signals. When tau becomes chemically altered, it detaches from this scaffolding and tangles into dense, insoluble fibers inside the cell. Without functioning tau, the cell’s transport system collapses. Neurons starve and die, and the tangles spread from one brain region to the next over a period of years.
This damage typically begins in areas of the brain responsible for forming new memories, which is why short-term memory loss is usually the earliest noticeable symptom. Over time, the destruction spreads to regions that control language, spatial awareness, reasoning, and eventually basic bodily functions like swallowing and walking.
Vascular Dementia: When Blood Flow Is the Problem
Vascular dementia is the second most common form. Instead of rogue proteins, the culprit here is reduced blood flow to the brain. Brain cells need a constant supply of oxygen and nutrients. When that supply is disrupted, cells die.
This can happen suddenly after a stroke, when a blood clot blocks an artery or a vessel bursts and causes bleeding. Whether thinking and memory are affected depends on the severity of the stroke and where in the brain it occurs. Some people develop dementia after a single large stroke. Others experience a series of smaller strokes over time, each one damaging a different part of the brain.
Vascular dementia can also develop gradually without a dramatic stroke event. Atherosclerosis, where cholesterol and other substances build up inside artery walls, slowly restricts blood flow to the brain. Damage to the small blood vessels and nerve fibers deep in the brain’s white matter is another common pattern, sometimes called subcortical ischemic vascular dementia. The cognitive decline in these cases tends to be slower and more stepwise than in Alzheimer’s, often affecting concentration and processing speed before memory.
Lewy Body Dementia and Frontotemporal Dementia
Lewy body dementia involves a different misfolded protein called alpha-synuclein. This protein can adopt several abnormal shapes, and depending on which shape it takes, it causes different diseases. In Lewy body dementia, alpha-synuclein deposits form inside brain cells and disrupt their function. The same protein, in a different configuration, also drives Parkinson’s disease, which is why the two conditions share features like movement stiffness and tremors. Lewy body dementia is particularly notable for visual hallucinations, fluctuating alertness throughout the day, and sleep disturbances that can begin years before memory problems appear.
Frontotemporal dementia is less common but strikes earlier in life, often between ages 45 and 65. It targets the frontal and temporal lobes, the parts of the brain responsible for personality, behavior, and language. About half of people with frontotemporal dementia have abnormal tau buildup in the brain. The other half have accumulations of a different protein called TDP-43, and a small fraction (roughly 5 percent) have deposits of a third protein called FUS. Because the frontal lobe governs social behavior and impulse control, the earliest signs are often personality changes, loss of empathy, or compulsive behavior rather than memory loss.
Mixed Dementia Is More Common Than Most People Realize
Many people assume dementia has a single, clean cause. Autopsy studies tell a different story. Research from the National Institute on Aging found that mixed pathologies, meaning two or more types of brain damage occurring together, were present in 45 percent of people who had dementia. Among people with three or more types of brain pathology, 95 percent had dementia. By contrast, only 22 percent of people with no detectable brain pathology showed signs of cognitive decline.
The most common combination is Alzheimer’s disease plus vascular damage, but Lewy body changes and Alzheimer’s pathology also frequently overlap. This matters because it helps explain why dementia progresses differently in different people and why treatments targeting a single mechanism have had limited success. The older a person is at the time of death, the more likely their dementia involved multiple overlapping causes.
Risk Factors You Can and Can’t Control
Age is the single strongest risk factor for dementia, but it is not a cause in itself. Genetics also play a role. A gene variant called APOE e4 increases the risk of Alzheimer’s and is associated with developing the disease at a younger age. Carrying two copies of this variant raises the risk more than carrying one. Still, many people with APOE e4 never develop dementia, and many people without it do.
A landmark 2024 report from the Lancet Commission identified 14 modifiable risk factors that collectively account for a substantial share of dementia cases worldwide. These include less education in early life, hearing loss, high blood pressure, smoking, obesity, depression, physical inactivity, diabetes, excessive alcohol consumption, traumatic brain injury, air pollution, social isolation, untreated vision loss, and high LDL cholesterol. The last two, vision loss and cholesterol, were added based on newly compelling evidence.
None of these factors guarantee dementia on their own, but they stack. A person with untreated hearing loss, high blood pressure, limited physical activity, and social isolation carries significantly more risk than someone who addresses those issues. The practical takeaway is that while you cannot change your age or your genes, a meaningful portion of dementia risk is shaped by health conditions and lifestyle factors that respond to intervention, often decades before symptoms would appear.
Conditions That Mimic Dementia
Not all cognitive decline is permanent. Vitamin B12 deficiency, certain medications, severe depression, and chronic sleep deprivation can all produce symptoms that look like dementia, including confusion, memory lapses, and difficulty concentrating. These conditions are sometimes called “reversible dementias,” though “treatable causes of cognitive impairment” is more accurate, since the underlying brain diseases that cause true dementia cannot currently be reversed.
Thyroid disease has long been considered a potential contributor to cognitive decline, and doctors routinely order thyroid tests during dementia evaluations. However, a large body of recent research has found no clear statistical link between thyroid dysfunction and dementia risk. Treating thyroid conditions, whether overactive or underactive, has not been shown to improve brain function in clinical trials. This doesn’t mean thyroid health is unimportant, but it does mean that thyroid problems are unlikely to be the explanation for significant memory or thinking changes.
If cognitive symptoms come on quickly, over weeks or months rather than years, or if they coincide with starting a new medication or a period of poor nutrition, it is worth investigating reversible causes before assuming the worst. The distinction matters because these conditions respond to treatment, and the cognitive problems they cause often improve or resolve completely.