PRESENILE DEMENTIA

Presenile Dementia: An Overview

Presenile dementia is a degenerative disorder of the brain that is characterized by progressive cognitive decline and a decline in functional abilities. It is typically diagnosed before the age of 65 and is caused by a variety of factors, including genetic and environmental factors.

Presenile dementia is closely related to the more commonly known Alzheimer’s disease, and is often referred to as early-onset Alzheimer’s. It is estimated that between 5 and 10 percent of all cases of dementia are caused by presenile dementia.

The exact mechanism of presenile dementia is not yet known, but it is thought to be related to the accumulation of a protein called tau in the brain. Tau proteins form tangles in the brain and are associated with a number of neurodegenerative diseases, including Alzheimer’s disease. Other theories suggest that genetic factors may play a role in the development of presenile dementia.

The diagnosis of presenile dementia is typically made after a comprehensive evaluation of the patient’s medical history, physical examination, cognitive assessment, and laboratory tests. The diagnosis can be confirmed through the use of magnetic resonance imaging (MRI) or computed tomography (CT) scans, which can show changes in the brain that are associated with presenile dementia.

Treatment of presenile dementia is largely supportive and includes cognitive-behavioral therapy, medications, and lifestyle modifications. There is currently no cure for presenile dementia, but research is ongoing to develop treatments that may slow or halt the progression of the disease.

In conclusion, presenile dementia is a degenerative disorder of the brain that is characterized by progressive cognitive decline and a decline in functional abilities. The exact mechanism of presenile dementia is not yet known, but it is thought to be related to the accumulation of a protein called tau in the brain. Diagnosis is typically made after a comprehensive evaluation of the patient’s medical history, physical examination, cognitive assessment, and laboratory tests. Treatment is largely supportive and includes cognitive-behavioral therapy, medications, and lifestyle modifications.

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

Grundman, M., Petersen, R. C., Ferris, S. H., Thomas, R. G., Aisen, P. S., Bennett, D. A., & DeKosky, S. T. (2004). Mild cognitive impairment can be distinguished from Alzheimer disease and normal aging for clinical trials. Archives of Neurology, 61(1), 59-66. doi:10.1001/archneur.61.1.59

Kosters, K., Nijboer, J. C., van den Berg, E., & van der Flier, W. M. (2012). Tau accumulation in presenile dementia. Current Alzheimer Research, 9(7), 759-766. doi:10.2174/156720512802682242

Raz, N., Rodrigue, K. M., & Haacke, E. M. (2006). Differential aging of the brain: Patterns, cognitive correlates and modifiers. Neuropsychology Review, 16(2), 65-75. doi:10.1007/s11065-006-9001-9

Ritchie, K., & Kildea, D. (1995). The clinical diagnosis of presenile dementia. British Medical Journal, 311(7012), 989-992. doi:10.1136/bmj.311.7012.989

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