Dementia

Dementia Support   Types   Symptoms   Causes  

Types of Dementia

Vascular Dementia

Vascular dementia (multi-infarct dementia), second only to Alzheimer’s, is a general term referring to difficulty in thought processes like reasoning and memory. It is caused by brain damage from poor circulation to the brain due to multiple conditions like a stroke, mini-stroke, or atherosclerosis. In addition, the person may be left with weakness down one side of the body or problems with vision or speech. If related to mini-strokes, each stroke can result in small patches of dead tissue in the cortex of the brain.

Subcortical Vascular Dementia.

Another version of vascular dementia is called subcortical vascular dementia resulting from deterioration of the small blood vessels deep in the brain. This often causes widespread damage to white matter beneath the cortex, affecting nerve fibers that carry signals between different parts of the cortex, including the frontal lobes. A person with subcortical vascular dementia will therefore often have slowed thinking and problems with executive function. The commonality of vascular dementia suggests that dyslipidemia is in the blood (containing an abnormal amount of lipids such as triglycerides, cholesterol, and/or fat phospholipids). Also, the results of having high cholesterol related to AD are mixed, and a number of studies reported that high total cholesterol levels increased risk of AD significantly1, 2

Dementia with Lewy Bodies

Lewy body dementia (DLB) is a progressive dementia third after Alzheimer’s in which protein deposits (Lewy bodies) accumulate within nerve cells in parts of the brain involving thinking, memory and movement, the cerebral cortex, limbic system, and brain stem. The brain of a person with DLB often shows less overall shrinkage than the brain of someone with Alzheimer's or frontotemporal dementia. In DLB, early damage is seen in the visual pathways and possibly also in the frontal lobes, which may explain why problems with vision and attention are commonly found as early symptoms of DLB. Similarly, Lewy bodies in the brain stem may be linked to the problems with movement.

Frontotemporal Dementia

In all forms of frontotemporal dementia (FTD), the frontal and/or temporal lobes shrink. The frontal lobes control emotional expression, memory, logic, language, judgment, and sexual behaviors. The temporal lobes, at the side behind the ears, he temporal lobes sit behind the ears play a role in processing emotions, language, and certain aspects of visual perception. If these lobes shrink the patient tends to repeat the same word, phrase, or action over and over again. Changes in the cortex also can result in the person becoming withdrawn and losing motivation. In the early stages, the person may have fluent speech but struggle to find the right word for something, or they may ask what a familiar word (example: ‘knife’) means. Damage to the right temporal lobe leads to problems recognizing faces and also objects.

Symptoms

Dementia isn’t a specific disease. Instead, dementia describes a group of symptoms affecting memory, thinking and social abilities severely enough to interfere with daily functioning.

Word-object problems. People experience difficulty in finding the right words or even recognizing common words as the relate to objects.

Difficulty in daily life. Patients experience difficulty with common tasks, organizing and planning, recognizing people they know, reasoning and problem-solving.

Motor functions. People have trouble with coordination and motor functions, being confused and disoriented.

Brain “fog” is a constellation of symptoms that include reduced mental acuity and cognition, inability to concentrate and multitask, as well as loss of short and long-term memory.

Psychological symptoms such as depression, anxiety, difficulty sleeping, agitation, paranoia, personality changes, and hallucinations.

Causes of Dementia

In addition to aging, a general lifestyle pattern appears to be a major risk factor for development of dementia. Risks include long-term consumption of high-fat, high-sucrose, refined-grains diet, poor nutrition and/or nutrient absorption, sedentary lifestyle, chronic insomnia, social isolation, chronic stress, cognitive inactivity, and epigenetic (environmental) factors.

More specifically, research points to genetic inheritance, cardiovascular and cerebrovascular problems, excessive alcohol consumption, traumatic brain injury, chronic inflammation, compromised blood-brain barrier, biochemical imbalances, oxidative stress, and having one or two copies of the APOE4 genetic variant.

General Causes

Aging. Neurodegeneration increases with age and is characterized by progressive deterioration of the structure and function of neurons, crucially accompanied by severe cognitive deficits.

Genetics. Family history of some forms of dementia is a strong factor.

Medications. including anticholinergic drugs (drugs that block the neurotransmitter acetylcholine in the central and the peripheral nervous system).3 These drugs are typically used to treat a variety of conditions such as including urinary incontinence, overactive bladder (OAB), chronic obstructive pulmonary disorder (COPD), and certain types of poisoning. Sleeping pills, anti-anxiety drugs, antidepressants, and some cold remedies can worsen dementia.

Diet and nutrition. Poor diet and/or poor absorption of essential nutrients is a factor. Deficiency or low levels in specific vitamins such as vitamin D3, and B vitamins can result in cognitive difficulty, mood swing, and depression. In contrast to the healthful effects of diets that are rich in omega-3 fatty acids and antioxidants, epidemiological studies indicate that diets with high contents of trans and saturated fats adversely affect cognition.4 A diet high in “junk food” and saturated fats elevates the neurological burden that is associated with brain injury, as evidenced by a worse performance in learning tasks and a reduction of BDNF-mediated synaptic plasticity.5, 6, 7 This type of diet increases the vulnerability of cells to damage8 by causing free-radical formation that surpasses cellular buffering capacity.

Nutrient deficiencies. Specific nutrient deficiencies such as zinc, vitamins B1, B2, B6, B12 and magnesium contribute to brain dysfunction. Zinc deficiency may induce learning and memory impairment. B12 deficiency has been linked to mental decline (which can often be mistaken for dementia). Magnesium is essential for learning and memory, and has been shown to support brain plasticity for optimal learning, memory, and cognitive function. It also suppresses amyloid beta build-up in the brain.

Lack of exercise. As one ages, we become more sedentary. Exercise helps maintain healthy circulation, supports ongoing detoxification, improves overall mood (reducing onset of depression), and helps keep us more mobile. It reduces inflammation, stimulates the brain to create new neural connections and helps improve insulin sensitivity. Daily running, fast walking, gym workouts, swimming, tennis, dancing are all good examples of good daily exercises.

Lack of social support. Mood may influence social behavior, and social support is one of the most studied psychosocial factors in relation to health and disease, possibly resulting in mimicking symptoms of dementia.

Sleep. Not getting enough sleep at night and chronic insomnia cause many cognitive and related problems.

Circadian rhythm. Related to sleep is the circadian rhythm which runs twenty-four hours and is often referred to as your “sleep/wake cycle.” Part of your hypothalamus controls your circadian rhythm which works best with regular sleep schedule habits. Circadian rhythms have regulatory effects on cell proliferation, cell metabolism, cell senescence, and cell death.

Chronic stress. Studies have shown that stress has many effects on the human nervous system and can cause structural changes in different parts of the brain (especially in the hippocampus), including the response to stress, cognition, behavior, and memory.9, 10

During extended periods of high stress, neuron growth decreases and the hippocampus can shrink in size.11 Both psychological and emotional stress, experienced over time causes the body to stay in a “flight and fight” mode, which can result in autoimmune disease, chronic inflammation, high blood pressure, high cholesterol, cardiovascular disease, stroke, digestive issues, fertility difficulties, depression, anxiety, memory (especially spatial memory),12 and cognitive problems, as well as behavioral, cognitive, and also mood disorders.13

Chronic mild stress can cause complications such as “increased IL-6 and plasma cortisol, as well as decreased amounts of cAMP responsive element binding protein and brain-derived neurotrophic factor (BDNF). This is very similar to what is observed in people with depression and mood disorders that exhibit a wide range of cognitive problems.”14

Oxidative stress. Free radical damage contributes to all types of disease. Cognitive decline is associated with increased oxidative stress, which may be partially responsible for the time-dependent accumulation of cellular damage,15 ultimately leading to neuronal death and neurodegenerative disorders.

Chronic Inflammation. Over time chronic inflammation can cause the immune system to go into overdrive, resulting in it attacking its own healthy cells.

Microglial cells in the brain, which are needed to break down redundant or dead nerve tissue, are part of the immune system. In development of dementia they fail to clear away waste. Chronic inflammatory conditions associated with autoimmune diseases show high microglial activity.

Chronic inflammation can also be caused by emotional stress; there is a physiological link between stress and mood-based cognitive disorders.16

Related Causes

Circulation

People with dementia seldom have just changes in their brains. One major condition often seen is vascular/cardiovascular problems which interfere with the free flow of oxygen and essential nutrients to the brain. In a person with dementia, a faulty blood-brain barrier prevents glucose from reaching the brain, allows pathogens and toxins to get to the brain, and prevents the clearing away of toxic beta-amyloid and tau proteins.

Strokes caused when a blood clot blocks the flow of blood to the brain, are the second most common cause of dementia, known medically as multi-infarct dementia. Studies have also found that baseline high density lipoprotein levels were lower and triglyceride levels were higher in elderly men who developed dementia with vascular components.17

Carotid atherosclerosis. The carotid artery supplies blood and oxygen to the brain. There is compelling evidence that carotid atherosclerosis is associated with brain atrophy. As we age, atherosclerosis occurs where accumulation of fat-laden, calcified plaque builds up in the blood vessels.18

Chronic high blood pressure in which blood vessels lose their elasticity cause the muscular layer of the vessels to enlarge, making it more difficult for the body to get the blood effectively to the brain. Hypertension may contribute to cognitive decline by causing cerebral small vessel pathology and increasing neurofibrillary tangles and amyloid plaques.19

Metabolic deficiencies or dysfunction

Cholinergic circuit dysfunction. The cholinergic circuit regulates memory and adaptability of the hippocampus through interactions with non-nerve cells. Problems of the cholinergic circuit, such as with the neurotransmitter acetylcholine, are important factors. Cholinergic circuit dysfunction has been associated with neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s as well as in psychiatric disorders such as schizophrenia.20

Seratonin is a chemical produced in the brain by nerve cells that is essential for nerve cell signaling. It is found mostly in the digestive system, although it’s also in blood platelets and throughout the central nervous system. Low levels of serotonin in the brain are linked to depression, anxiety, and sleep trouble.

Removal of ovaries. A Mayo Clinic study concluded that women whose ovaries are removed by the age of forty without having hormone replacement therapy, have double the risk of AD onset.21

Insulin imbalances. Messaging by insulin is essential for neuron survival and is compromised by chronically high levels of insulin. Insulin-degrading enzyme (IDE) is an enzyme responsible for the breakdown of insulin. IDE also degrades amyloid beta. If the IDE is tied up resolving excess insulin, there is less available to manage the levels of amyloid beta.22

High blood sugar levels, even in people without diabetes, are strongly linked to increased risk of dementia, and most specifically, Alzheimer's (which is sometimes called type 3 diabetes).23 Excess sugar also results in an increase of advanced glycation end products. These cause increases in free radicals and promote inflammation, damage blood vessels which can result in nutritional deficiencies in the brain.

Next: Dementia Support

Footnotes

1. Kivipelto M, Ngandu T, Fratiglioni L, Viitanen M, Kåreholt I, et al. (2005). Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Arch Neurol. Oct; 62(10):1556-60.
2. Whitmer RA, Sidney S, Selby J, Johnston SC, Yaffe K. (2005). Midlife cardiovascular risk factors and risk of dementia in late life. Neurology. Jan 25; 64(2):277-81.
3. Richardson K, Fox C, Maidment I, Steel N, Loke YK, et al. (2018). Anticholinergic drugs and risk of dementia: case-control study. BMJ. Apr 25;361:k1315.
4. Greenwood CE, Winocur G. (2005). High-fat diets, insulin resistance and declining cognitive function. Neurobiol Aging. Dec; 26 Suppl 1():42-5
5. Wu L, Sun D, He Y. (2017). Coffee intake and the incident risk of cognitive disorders: A dose-response meta-analysis of nine prospective cohort studies. Clin Nutr. 2017;36(3):730-6.
6. Vaynman S, Ying Z, Wu A, Gomez-Pinilla F. (2006). Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity. Neuroscience. 139(4):1221-34.
7. Wu A, Ying Z, Gomez-Pinilla F. (2004). The interplay between oxidative stress and brain-derived neurotrophic factor modulates the outcome of a saturated fat diet on synaptic plasticity and cognition. Eur J Neurosci. 19:1699–1707.
8. Mattson MP. (2005). Energy intake, meal frequency, and health: a neurobiological perspective. Annu Rev Nutr. 2005; 25():237-60.
9. 4 Lupien SJ, McEwen BS, Gunnar MR, Heim C. (2009). Effects of stress throughout the lifespan on the brain, behavior and cognition Nat Rev Neurosci. Jun; 10(6):434-45.
10. Lupien SJ, Lepage M. (2001). Stress, memory, and the hippocampus: can't live with it, can't live without it. Behav Brain Res. Dec 14; 127(1-2):137-58.
11. Squire, L.R, Schacter DL. (2002). The Neuropsychology of Memory. Guilford Press.
12. Borcel E, Pérez-Alvarez L, Herrero AI, Brionne T, Varea E, et al. (2008). Chronic stress in adulthood followed by intermittent stress impairs spatial memory and the survival of newborn hippocampal cells in aging animals: prevention by FGL, a peptide mimetic of neural cell adhesion molecule. Behav Pharmacol. Feb; 19(1):41-9.
13. Wang C, Wang W, Dong H, Hou P, et al. (2008). Chronic mild stress impairs cognition in mice: from brain homeostasis to behavior. Life Sci. Apr 23; 82(17-18):934-42.
14. Song L, Che W, Min-Wei W, Murakami Y, Matsumoto K. (2006). Impairment of the spatial learning and memory induced by learned helplessness and chronic mild stress Pharmacol Biochem Behav. Feb; 83(2):186-93.
15. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. (2013). The hallmarks of aging. Cell. Jun 6; 153(6):1194-217.
16. Solerte SB, Cravello L, Ferrari E, Fioravanti M. (2000). Overproduction of IFN-gamma and TNF-alpha from natural killer (NK) cells is associated with abnormal NK reactivity and cognitive derangement in Alzheimer's disease. Ann N Y Acad Sci. 917():331-40.
17. Stampfer MJ. (2006). Cardiovascular disease and Alzheimer's disease: common links. J Intern Med. Sep; 260(3):211-23.
18. Kin T, Yamano S, Sakurai R, Kajitani M, Okahashi Y, et al. (2007). Carotid atherosclerosis is associated with brain atrophy in Japanese elders. Gerontology. 53(1):1-6.
19. Den Heijer T, Launer LJ, Prins ND, van Dijk EJ, Vermeer SE, et al. (2005). Association between blood pressure, white matter lesions, and atrophy of the medial temporal lobe. Neurology. Jan 25; 64(2):263-7.
20. Tata AM, Velluto L, D'Angelo C, Reale M. (2014). Cholinergic system dysfunction and neurodegenerative diseases: cause or effect? CNS Neurol Disord Drug Targets. 2014;13(7):1294-303.
21. Rocca WA, Grossardt BR, Shuster LT, Stewart EA. (2012). Hysterectomy. Oophorectomy, estrogen, and risk of dementia. Neurodegenerative Disease 10: 175-178.
22. Schilling MA. (2016). Unraveling Alzheimer's: Making Sense of the Relationship between Diabetes and Alzheimer's Disease. J Alzheimers Dis. 2016;51(4):961-77.
23. Tups A, Benzler J, Sergi D, Ladyman SR, Williams LM. (2017). Central Regulation of Glucose Homeostasis. Compr Physiol. Mar 16;7(2):741-764.