Abstract
All traumas—cranial, cardiovascular, hormone, viral, bacterial, fungi, parasites, misfolded protein, genetic, behavior, environmental and medication—affect the brain. This paper itemizes studies showing the many different causes of dementia including Alzheimer’s disease. Causes interact with each other, act sequentially by preparing the optimal conditions for its successor, initiate other diseases, allow for other traumas to accumulate and degrade protective features of the brain. Since such age-related cognitive impairment is not exclusively a human attribute there might be support for an evolutionary theory of dementia. Relying on theories of antagonistic pleiotropy and polymorphism, the brain has been designed to sequester trauma. Because of increased longevity, the short-term tactic of sequestering trauma becomes a long-term liability. We are engineered to sequester these insults until a tipping point is reached. Dementia is an evolutionary trade-off for longevity. We cannot cure dementia without understanding the overall biology of aging.
Highlights
All traumas—cranial, cardiovascular, hormone, viral, bacterial, fungi, parasites, misfolded protein, genetic, behavior, environmental and medication—affect the brain
This review found that the following were all associated with increased risks of progression of mild cognitive impairment (MCI) to dementia; hypertension; adiposity; cholesterol; and Glycaemic control
The studies collated under this review present a foundation for a serious discussion about the concept—how we think of—and construct—how we measure—dementia
Summary
We must first define and understand the causes of each variant of the disease. Despite more than a century of mistakenly looking at amyloid plaques followed by neurofibrillary tangles, we have again started questioning alternate causes of dementias. Such enlightenment did not come by an orderly and coordinated national neurobiological research Guidelines [1] or Framework [2]. More than 95 percent of cases of dementia are attributable to Alzheimer's disease, vascular dementia, Lewy body, and frontotemporal dementia. Degenerative causes: Familial Alzheimer’s disease; Pure hippocampal sclerosis; frontotemporal lobar degeneration; primary progressive (non-fluent) aphasia; Semantic dementia; Progressive supranuclear palsy Richardson–Olszewsky syndrome); Corticobasal degeneration; Multiple system atrophy (Shy–Drager syndrome); Amyotrophic lateral sclerosis/motor neuron disease (Lou Gehrig’s disease); Huntington’s disease; Ataxias (spinocerebellar ataxias, Friedreich’s ataxia); Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy-Nasu–Hakola disease; Wilson disease; neuronal ceroid lipofuscinoses-Kufs disease; Gaucher disease (2 and 3); Fragile X syndrome; Fabry disease; Limbic encephalitis (LATE); Niemann–Pick disease Type C; and Spinocerebellar ataxia
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