Almost half of dementia is easily preventable.

Vascular cognitive impairment is the dementia most directly tied to blood flow: stiffened, leaky small vessels dysregulate perfusion, the white matter is injured, and the resulting white-matter lesions predict future dementia, raising the risk of the vascular kind by about 73 percent across a 36-study review of 19,040 people.² On its own it is the second most common dementia, roughly 15 to 20 percent of cases, but the true vascular contribution is far larger once mixed pathology is counted, since vascular damage turns up in up to about half of Alzheimer brains.³ Because the cause is vascular, it is preventable: in SPRINT-MIND, targeting systolic blood pressure under 120 slowed white-matter-lesion growth and cut mild cognitive impairment.⁴⁵ Two caveats: SPRINT-MIND stopped early and never proved a drop in full dementia by itself; and since most older brains carry mixed pathology, treating blood pressure lowers risk and slows the damage without promising any one person escapes dementia.

In Alzheimer’s, low brain blood flow appears early. ASL and SPECT imaging show reduced perfusion in the posterior cingulate, precuneus and temporoparietal cortex, often before atrophy or symptoms appear, with parietal flow already falling at the mild-cognitive-impairment stage and down by roughly a quarter by the dementia stage.⁶⁷ The small vessels and the blood-brain barrier start leaking early, beginning in the hippocampus, and this damage predicts later cognitive decline even when amyloid and tau still look normal, especially in carriers of the APOE4 gene.⁸⁹ Controlling vascular risk is one reason the 2024 Lancet Commission estimates that addressing modifiable factors, several of them vascular, could prevent or delay around 45 percent of dementia.¹ Low flow is part cause and part consequence, because the brain throttles supply as neurons fail, and Alzheimer’s has many drivers beyond its vessels.¹⁰ It also skews female, about two in three patients are women.¹¹ The loss of estrogen, a vasodilator that helps hold the small vessels open, is one contributor alongside the longer female lifespan, see the hormone story.

In DLB, blood flow and metabolism drop in the occipital lobes at the back of the brain, often while a patch of posterior cingulate stays relatively spared (the cingulate island sign). That back-of-brain pattern is the single most useful feature separating DLB from Alzheimer’s on perfusion SPECT and FDG-PET, and it is written into the formal diagnostic criteria.¹²¹³ But the low flow is a downstream consequence of alpha-synuclein (Lewy body) pathology, not a vascular cause, and the occipital cortex itself is largely intact, functionally silenced by lost inputs rather than destroyed, which is why dopamine-transporter imaging is a far stronger marker than blood flow.¹⁴ Because DLB and Parkinson’s disease dementia are the same synucleinopathy, their imaging patterns are hard to tell apart.¹⁵

Parkinson’s is primarily a disease of dopamine-making cells and misfolded alpha-synuclein, but the brain’s blood supply gets pulled in. Imaging shows the cortex running underperfused, strongest toward the back of the brain, and this deepens once Parkinson’s progresses to dementia.¹⁶¹⁷ On top of this, about one in three people with Parkinson’s has orthostatic hypotension, so standing drops their blood pressure and pulls brain blood flow down with it, causing dizziness, foggy moments and falls.¹⁸¹⁹ Comorbid small-vessel damage adds to it, and regular aerobic exercise has the best evidence for protecting both flow and function.²⁰ One caveat: in Parkinson’s the perfusion changes mostly follow the neurodegeneration and feed back on it, rather than starting it.