LATE is a term that describes a prevalent medical condition with impaired memory and thinking in advanced age, often culminating in the dementia clinical syndrome. In other words, the symptoms of LATE are similar to those of Alzheimer's disease. The acronym LATE stands for Limbic-predominant Age-related TDP-43 Encephalopathy. "Limbic" is related to the brain areas first involved, "age-related" and the name "LATE" itself refer to the onset of disease usually in persons aged 80 or older. "TDP-43" indicates the aberrant mis-folded protein (or proteinopathy) deposits in the brain that characterize LATE, and "encephalopathy" means illness of brain. At present, LATE can only be diagnosed with certainty at Autopsy. The terminology used to refer to the brain changes identified in autopsy-confirmed LATE is: LATE neuropathologic change (LATE-NC). The diagnosis of LATE-NC at autopsy requires detection of pathologic TDP-43 protein deposits in the brain. For reasons that are presently unknown, the disease process of LATE-NC preferentially affects medial temporal lobe structures of the brain, particularly the amygdala and hippocampus. In a significant proportion of persons with LATE-NC, there is atrophy, cell loss and astrogliosis in the hippocampus, diagnosable at autopsy (and somewhat less specifically via MRI during life) as hippocampal sclerosis. Brains with LATE-NC and hippocampal sclerosis are relatively more affected clinically than those with LATE-NC alone. LATE is a very common condition: autopsy studies around the world indicate that LATE-NC is present in the brains of about one-third of people over 85. LATE typically affects persons older than 75 years of age (with some exceptions; please see below) and becomes increasingly prevalent every year in advanced old age. This is in contrast to Alzheimer's disease, which tends to level off and even decrease in prevalence among persons beyond age 85 years. LATE is often comorbid with (i.e., occurs in the same brain as) other pathologic changes that are also associated with dementia, such as Alzheimer's disease and cerebrovascular disease(s). LATE has a large impact on public health. Clinical-pathologic correlation studies have established that the presence of LATE-NC is associated with impairments in memory and thinking. In older persons whose brains lack Alzheimer's disease-type amyloid plaques and neurofibrillary tangles, the presence of LATE-NC at autopsy is associated with a relatively slow cognitive decline (in comparison with Alzheimer's disease), mostly affecting the memory domain. However, most people (~75%) beyond age 85 have some Alzheimer's disease-type pathology and in this common scenario the impact of LATE-NC is very important. Approximately one-half of persons with Alzheimer's disease pathology also have LATE-NC. In these persons, the presence of LATE-NC is associated with a swifter disease course and with more severe clinical (memory and thinking) impairment than when only Alzheimer's disease pathology is present. A common combination of brain pathologies—with Alzheimer's disease pathology, Lewy body pathology, and LATE-NC in the same brain—tends to affect younger individuals (often <75 yrs of age) and, on average, is associated with more aggressive (faster) cognitive deterioration. With or without co-existing Alzheimer's disease or other brain changes, persons with LATE-NC generally lack the clinical features of frontotemporal dementia (FTD).
Signs and symptoms
Cognitive symptoms The hallmark symptom of LATE is a progressive memory loss that predominantly affects short-term and episodic memory. This impairment is often severe enough to interfere with daily functioning and usually remains the chief neurologic deficit, unlike other types of dementia in which non-memory cognitive domains and behavioral changes might be noted earlier or more prominently. The amnestic syndrome in LATE tends to worsen gradually, leading to significant memory deficits and functional disability over time. Thus, the cognitive decline in LATE, when LATE-NC is the chief illness present, is typically relatively slow. The term dementia refers to a clinical syndrome, rather than a particular disease process – dementia can be caused by many different subtypes of brain disease, which often occur in combination with each other. The specific implication of the term dementia is that, in the affected individual, there is cognitive impairment severe enough to impair activities of daily living such as feeding oneself. Many diseases in addition to Alzheimer's disease and LATE can (by harming brain function) contribute to the dementia clinical syndrome, and often occur in combination. For example, vascular factors ("stroke" and other blood vessel-affecting conditions, driven by such risk factors as hypertension and diabetes) and other brain diseases can cause or worsen dementia in human populations. However, up to half of severe dementia in advanced age includes both Alzheimer's disease and LATE-NC pathologies, and people with these co-pathologies are at risk for relatively swift and severe disease course.[2]
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