White matter changes (WMCs) have been reported to be associated with a decline in motor function in speed and fine motor coordination, and with many diseases including AD [2,5,6], vascular dementia, dementia with Lewy bodies, and psychiatric disorders [5].
Unlike Alzheimer's disease, which shrinks the hippocampus causing progressive memory loss, white matter disease is a more diffuse mind-robbing condition that targets small blood vessels deep within the brain's white matter.
White matter disease is strongly linked to cardiovascular disease risk factors, and researchers believe that white matter disease is a biomarker (medical sign) of the lifelong risk of stroke, dementia and disability.
The difference between sub-cortical and white matter dementia occurs with procedural memory, which is impaired in subcortical dementia, but normal in white matter dementia as it is in cortical dementia. Thus, white matter dementia is seen as a memory retrieval deficit with normal procedural memory.
In general, the prognosis is grave, with the majority of patients dying after a few years. However, some die only after several months, and some manage to survive for several decades [6].
Four stages were defined by dividing individuals into simple quartiles corresponding to those with the lowest total WMSA (Quartile I, n = 25), mid-low total WMSA (Quartile II, n = 25), mid-high total WMSA (Quartile III, n = 25), and highest total WMSA (Quartile IV, n = 22) (Fig.
This is your brain on aging
By age 60, this degeneration, termed white matter disease, is present in more than half of the population.
Age-related white matter disease is progressive, meaning it can get worse. But you can take steps to stop it from spreading. Scientists think you might even be able to repair the damage, if you catch it early. Keep your blood pressure and blood sugar in check.
White matter lesions (WMLs) are areas of abnormal myelination in the brain. These lesions are best visualized as hyperintensities on T2 weighted and FLAIR (Fluid-attenuated inversion recovery) sequences of magnetic resonance imaging. They are considered a marker of small vessel disease.
They are very common in the aging brain, with an in‐life prevalence of over 90% in the over‐65 age group, the volume of lesions increasing with age group in the over‐60s 15, 42. Although often an incidental finding, they are clinically significant.
Magnetic resonance imaging (MRI)
Repeat scans can show how a person's brain changes over time. Evidence of shrinkage may support a diagnosis of Alzheimer's or another neurodegenerative dementia but cannot indicate a specific diagnosis. MRI also provides a detailed picture of brain blood vessels.
Higher functions like language and memory are organized into networks in which gray matter regions are connected by white matter tracts. The more extensive and efficient those connections, the better the brain works.
White matter abnormalities not only represent an early neuropathological event in Alzheimer's disease but may also play an important role in the pathogenesis and diagnosis of Alzheimer's disease.
White matter disease may develop with conditions associated with aging, such as stroke, but it can also affect young people due to conditions such as cerebral adrenoleukodystrophy and multiple sclerosis (MS).
White matter disease in midlife is heritable, related to hypertension, and shares some genetic influence with systolic blood pressure.
The prognosis of white matter disease varies. MS is not a fatal disease. By managing the MS and co-occurring conditions, life expectancy may be only slightly shorter. Vascular dementia generally is associated with a reduced life expectancy after diagnosis.
White matter dynamically changes in response to learning, stress, and social experiences. Several lines of evidence have reported white matter dysfunction in psychiatric conditions, including depression, stress- and anxiety-related disorders.
White matter injuries are very serious, but, depending on the type and extent of the injury, extensive recovery may occur. As long as the neuron cell bodies remain healthy, axons can regrow and slowly repair themselves.
White matter disease is a progressive disorder caused by age-related decline in the part of the nerves (the white matter) that connect different areas of brain to each other and to the spinal cord. This disorder can result in memory loss, imbalance and can lead to problems with mobility in older age.
Brain white matter (WM), and more specifically neuronal connectivity, is thought to perform a crucial role in the central processing of fatigue [1].
In contrast, human neuroimaging studies have generally found that alcohol is associated with deleterious changes in the brain including global and regional brain shrinkage and white matter damage, with frontal lobes being particularly affected (Oscar-Berman and Marinkovic, 2007; Sullivan et al., 2010).
White matter (WM) changes are often found in patients with vascular dementia, especially of small vessel/subcortical subtypes, including Binswanger's disease, and are generally considered to be a consequence of chronic ischemia associated with microangiopathy.
International studies revealed a significantly higher prevalence of depressive disorders in people with white matter lesions (WMLs) than in health (1–3). Additionally, the correlation between white matter alterations in various parts of the brain and depressive disorder is different (4).
Patients with extensive white matter hyperintensities are likely to have tension-type headaches or to have headaches develop during middle age, according to results published in Cephalagia. Currently, there are no established treatments or strategies for managing white matter hyperintensities.