Alzheimer's disease is the name given to the end state of rising amyloid levels in the brain: it is the stage at which the patient has a lot of amyloid and is severely impacted by it. But we will all suffer increased levels of amyloid to some degree, and we will all be negatively affected by it to some degree. This is similarly the case for the other protein aggregate involved in Alzheimer's disease, tau, that precipitates into tangles in brain tissue. Rising levels are a shared manifestation of aging, it is just that some people arrive at the pathological level much earlier. One of the objectives of repair based treatments that fix damaged clearance mechanisms or remove protein aggregates from tissues is to make this difference irrelevant - everyone should undergo the therapies every so often, and then no-one would have to worry about a future involving degeneration of the mind:
We recommend a new term, "primary age-related tauopathy" (PART), to describe a pathology that is commonly observed in the brains of aged individuals. Many autopsy studies have reported brains with neurofibrillary tangles (NFTs) that are indistinguishable from those of Alzheimer's disease (AD), in the absence of (Aβ) plaques. For these "NFT+/Aβ-" brains, for which formal criteria for AD neuropathologic changes are not met, the NFTs are mostly restricted to structures in the medial temporal lobe, basal forebrain, brainstem, and olfactory areas (bulb and cortex).
Symptoms in persons with PART usually range from normal to amnestic cognitive changes, with only a minority exhibiting profound impairment. Because cognitive impairment is often mild, existing clinicopathologic designations, such as "tangle-only dementia" and "tangle-predominant senile dementia", are imprecise and not appropriate for most subjects. PART is almost universally detectable at autopsy among elderly individuals, yet this pathological process cannot be specifically identified pre-mortem at the present time.
Improved biomarkers and tau imaging may enable diagnosis of PART in clinical settings in the future. Indeed, recent studies have identified a common biomarker profile consisting of temporal lobe atrophy and tauopathy without evidence of Aβ accumulation. For both researchers and clinicians, a revised nomenclature will raise awareness of this extremely common pathologic change while providing a conceptual foundation for future studies.