Dementia is an umbrella term that describes a range of neurological conditions that cause a decline in cognitive function. It impacts memory, thinking, problem solving, language, and behavior, significantly affecting one’s daily life. This blog delves into how dementia affects the brain, the neurological changes involved, and some of the causes of this debilitating condition.
How does dementia affect the brain?
Dementia is a clinical syndrome that results from various underlying brain disorders. The brain is a complex organ that undergoes specific changes in individuals with dementia, leading to the symptoms commonly observed. These changes vary depending on the type of dementia, but generally involve the loss of neurons and the connections between these neurons.
Neurons, which are the brain cells responsible for transmitting information, degrade at an accelerated rate in individuals with dementia, disrupting communication within the brain and impairing its ability to function correctly. Brain atrophy, or shrinkage of the brain, is a common phenotype in dementia, with regions such as the hippocampus and cerebral cortex shrinking significantly [1]. This atrophy often correlates with the severity of cognitive decline [1].
In Alzheimer’s disease (the most common form of dementia), two abnormal structures are typically found: amyloid plaques and neurofibrillary (tau) tangles. Amyloid plaques are clumps of protein fragments that accumulate between neurons, while tau tangles are twisted fibers, consisting of proteins, that build up inside neurons. Both amyloid plaques and tau tangles can disrupt cell function and contribute to neuronal damage and death [2]. Although this is the general consensus in reported studies, further studies are warranted to elucidate the exact sequence of events that leads to dementia.
What are the different types of dementia?
Understanding the specific neurological changes in dementia is essential for diagnosing and developing potential treatments. For example, in Alzheimer’s disease, amyloid plaques and tau tangles are hallmarks, with the hippocampus being one of the first regions affected, generally leading to early memory loss. As the disease progresses, other parts of the brain also become involved, resulting in more pronounced cognitive and behavioral symptoms.
Vascular dementia is caused by reduced blood blow to the brain, often due to a stroke causing damage to blood vessels. This leads to neuronal cell death and loss of brain tissue, particularly in areas critical for attention, reasoning, and memory. Symptoms can vary depending on the location and severity of the blood vessel damage, but they often include difficulties with problem solving, slowed thinking, and loss of focus [3].
Lewy body dementia is characterized by the presence of Lewy bodies, which are abnormal deposits of a protein called alpha synuclein, in the brain [4]. These deposits disrupt normal brain function, leading to symptoms that overlap with both Alzheimer’s and Parkinson’s disease, including movement problems, visual hallucinations, and cognitive decline.
Frontotemporal dementia primarily affects the frontal and temporal lobes of the brain (hence its name) leading to changes in personality, behaviour, and language. Consequently, individuals with frontotemporal dementia exhibit significant changes in personality and behaviour, such as apathy and impulsiveness. However, unlike other types of dementias, memory is often preserved in the early stages of frontotemporal dementia.
Mixed dementia involves a combination of characteristics from different types of dementia, most commonly Alzheimer’s and vascular dementia. This can lead to a more complex presentation of symptoms and faster progression of cognitive decline. Mixed dementia is particularly challenging to diagnose and treat due to the overlapping features and compounded effects on brain function.
What are the neurological changes that happen in dementia?
Dementia results from a plethora of causes, involving a combination of genetic, environmental, and lifestyle factors. Genetics can significantly influence the risk of developing dementia, with mutations in certain genes (such as PSEN1, PSEN2, and APP) contributing to Early Onset Alzheimer’s disease which can affect people in their 40s and 50s [5]. On the contrary, additional genes such as APOE ε4 allele is a well-known genetic risk factor for late onset Alzheimer’s Disease [6].
Conditions that affect the blood vessels, such as hypertension, diabetes, and high cholesterol, increase the risk of vascular dementia. These conditions can lead to strokes or other forms of brain damage, contributing to cognitive decline. Managing these risk factors through lifestyle changes and medication can reduce the risk of developing dementia.
Additionally, lifestyle choices such as diet, exercise, smoking and alcohol consumption, impact brain health. A healthy diet and lifestyle can lower the risk of dementia significantly. Environmental factors, such as exposure to toxins or head injuries, can also play a role in developing dementia. Repeated head trauma has been linked to chronic traumatic encephalopathy (CTE), a form of dementia [7].
Certain medical conditions like Parkinson’s disease, Huntington’s disease, and multiple sclerosis, can further increase the risk of developing dementia. Additionally, severe depression and untreated sleep apnea have been associated with an increase of cognitive decline. Addressing these conditions through appropriate medical care and lifestyle modifications is crucial for reducing the risk of dementia [7].
Conclusion
Dementia profoundly impacts the brain, leading to a decline in cognitive function and quality of life. By understanding the neurological changes and causes of dementia, researchers and healthcare professionals can develop better strategies for diagnosis, treatment, and prevention. Ongoing research continues to uncover new insights into the complex mechanisms of dementia, offering hope for future breakthroughs in managing and potentially curing this challenging condition. As our understanding of dementia evolves, our capacity to support those affected by the condition also grows, ultimately enhancing the quality of life for both patients and their caregivers.
References
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[2]. Kumar A, Sidhu J, Lui F, et al. Alzheimer Disease. [Updated 2024 Feb 12]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499922/.
[3]. Sanders AE, Schoo C, Kalish VB. Vascular Dementia. 2023 Oct 22. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 28613567.
[4]. Simon, C., Soga, T., Okano, H.J. et al. α-Synuclein-mediated neurodegeneration in Dementia with Lewy bodies: the pathobiology of a paradox. Cell Biosci 11, 196 (2021). https://doi.org/10.1186/s13578-021-00709-y.
[5]. Xiao X, Liu H, Liu X, Zhang W, Zhang S, Jiao B. APP, PSEN1, and PSEN2 Variants in Alzheimer’s Disease: Systematic Re-evaluation According to ACMG Guidelines. Front Aging Neurosci. 2021 Jun 18;13:695808. doi: 10.3389/fnagi.2021.695808. PMID: 34220489; PMCID: PMC8249733.
[6]. Breijyeh Z, Karaman R. Comprehensive Review on Alzheimer’s Disease: Causes and Treatment. Molecules. 2020 Dec 8;25(24):5789. doi: 10.3390/molecules25245789. PMID: 33302541; PMCID: PMC7764106.
[7]. Livingston G, Huntley J, Sommerlad A, Ames D, Ballard C, Banerjee S, Brayne C, Burns A, Cohen-Mansfield J, Cooper C, Costafreda SG, Dias A, Fox N, Gitlin LN, Howard R, Kales HC, Kivimäki M, Larson EB, Ogunniyi A, Orgeta V, Ritchie K, Rockwood K, Sampson EL, Samus Q, Schneider LS, Selbæk G, Teri L, Mukadam N. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet. 2020 Aug 8;396(10248):413-446. doi: 10.1016/S0140-6736(20)30367-6. Epub 2020 Jul 30. Erratum in: Lancet. 2023 Sep 30;402(10408):1132. doi: 10.1016/S0140-6736(23)02043-3. PMID: 32738937; PMCID: PMC7392084.
