I. Causes of Dementia
C. Diseases Causes of Dementia
C.1. Alzheimer's disease
Alzheimer's disease is a brain disorder named for German physician Alois Alzheimer. Alzheimer's destroys brain cells, causing problems with memory, thinking and behavior severe enough to affect language communication, memory, lifelong hobbies or social life. Alzheimer's gets worse over time, and it is fatal. Over 1 million people in US alone are currently afflicted by Alzheimer's disease because of degeneration of hippocampus and cerebral cortex of the brain where memory, language and cognition are located. With this mental disorder, brain cells gradually die and generate fewer and fewer chemical signals day by day resulting in diminished of functions. Overtime memory thinking as well as behavior deteriorates. Today, there is no known cure.
C.2. Stroke (Vascular problems)Strokes are caused by uncontrolled diet that is high in saturated and trans fats as a result of bad cholesterol building up in the blood vessels that block the circulation of blood to the body including the brain. If oxygen is not delivered to the brain cells, some cells die off and can not reproduce, then you may get a stroke. Other happen when a blood vessel in the brain ruptures causing the cells in your brain deprived of oxygen that can lead to symptoms of vascular dementia.
In atudy of Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis, conducted by University Department of Clinical Neurology, John Radcliffe Hospital, Dr. Pendlebury ST, Rothwell PM. showed that 10% of patients had dementia before first stroke, 10% developed new dementia soon after first stroke, and more than a third had dementia after recurrent stroke. The strong association of post-stroke dementia with multiple strokes and the prognostic value of other stroke characteristics highlight the central causal role of stroke itself as opposed to the underlying vascular risk factors and, thus, the likely effect of optimum acute stroke care and secondary prevention in reducing the burden of dementia.(1)
C.3. Dementia with Lewy bodies
Lewy bodies is defined as a spherical masses that displace other cell components. Abnormal aggregates of protein develop inside nerve cells found in Parkinson's disease (PD), Lewy Body Dementia and some other disorders.(2). In teh study to identify the patterns of diffusivity changes in patients with dementia with Lewy bodies (DLB) and Alzheimer disease (AD) and to determine whether diffusion tensor MRI (DTI) is complementary to structural MRI in depicting the tissue abnormalities characteristic of DLB and AD, the team at Mayo Clinic, found that increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala. Diffusivity measurements were complementary to structural MRI, demonstrating that measures of diffusivity on diffusion tensor MRI are valuable tools for characterizing the tissue abnormalities characteristic of Alzheimer disease and DLB.(3)
C.4. Fronto-temporal dementia
Fronto-temporal dementia (FTD) or Pick's disease is defined as the clinical syndrome caused by degeneration of the frontal lobe of the brain. Although early diagnosis of fronto-temporal dementia (FTD) is often difficult because of the non-specific presentation, some researchers showed that the inhibition of reflexive and voluntary saccades appears to be independently processed. A delayed antisaccade task could be useful for the early diagnosis of FTD.(4). Others suggested depression and executive dysfunction triggers the loss of autonomy, the risk of fall and of malnutrition in elderly patients. The clinical significance of this study is that the delineation of specific executive in depressed elderly patients may facilitate the development of effective treatment interventions, including treatment for geriatric depression.(5)
C.5. Progressive supranuclear palsy
Progressive supranuclear palsy is defined as a condition of a movement disorder occurred as a result of damage to certain nerve cells in the brain that lead to serious and progressive problems with control of gait and balance, including an inability to aim the eyes properly. In a study to observe the progressive supranuclear palsy syndrome (PSPS) and corticobasal syndrome (CBS) and associated with relatively specific patterns of atrophy; the former predominantly involving the brainstem, the latter frontoparietal regions, in a 41 subjects and controls study, by utilizing the technique of voxel-based morphometry to assess both gray and white matter volume loss in six prospectively recruited Hybrids that underwent 3.0 T volumetric head magnetic resonance image scanning to determine the neuroanatomical correlates of the syndrome. he Hybrid group showed imaging features of both PSPS and CBS, with volume loss observed in the brainstem (superior cerebellar peduncle) and cortex (medial and lateral premotor, prefrontal, and motor cortex). As expected, typical patterns of loss were observed in PSPS and CBS.(6)
Others suggested that The patients with CBDS displayed an asymmetric (left > right) pattern of brain atrophy that involved the bilateral premotor cortex, superior parietal lobules, and striatum. Progressive supranuclear palsy was associated with atrophy of the midbrain, pons, thalamus, and striatum, with minimal involvement of the frontal cortex. Midbrain structures were more atrophied in PSP than in CBD, whereas dorsal frontal and parietal cortices were more atrophied in CBD than in PSP. The degree of atrophy of the midbrain and pontine tegmentum and the left frontal eye field differentiated the 2 patient groups with 93% accuracy.(7)
C.6. Korsakoff's syndrome
Korsakoff's syndrome, named after Sergei Korsakoff, a Russian neuropsychiatris is defined as a neurological disorder as a result of deficiency of Vitamin B1 (thiamine) in the brain and associated closely to chronic alcohol abuse and/or severe malnutrition. In the study The links between spatial behavior and hippocampal levels of synapsin I and phosphosynapsin in normal rats and in the pyrithiamine-induced thiamine deficiency (PTD) rat model of Wernicke-Korsakoff's syndrome, found that spontaneous alternation performance was impaired in PTD rats and was accompanied by a significant reduction (30%) in phosphorylated synapsin I(8). Other study comfirmed that confirms the widespread neurotoxic effect of chronic alcohol consumption. Only a few cerebral regions, including the medial thalami, mammillary bodies, and corpus callosum, were more severely damaged in KS than in AL. The continuum of macrostructural damage from AL to KS is therefore restricted to key brain structures. Longitudinal investigations are required to determine whether alcoholic patients with medial thalamic volumes that are comparable to those of patients with KS are at increased risk of developing KS.(9). Scientist at the University of Campinas (Unicamp),suggested that self-imposed long-lasting nutritional deprivation is thought to be the main cause of thiamine deficiency and subsequent encephalopathy, but adjunct factors, such as magnesium depletion and chronic alcohol misuse, might have played an important role, especially in the development of Korsakoff's syndrome(10)
C.7. Binswanger's disease
Binswanger disease also known as subcortical vascular dementia is defined as a type of small vessel vascular dementia caused by microscopic areas of damage to the deep layers of white matter in the brain, including mostly of glial cells and myelinated axons worked to transmit signals from one region of the cerebrum to another and between the cerebrum and lower brain centers. Binswanger's disease frequency increases with age independent of other risk factors, and in nondemented subjects leukoaraiosis is associated with deficits in selected cognitive functions.(11). Other clinical finding associated with Binswanger's disease are varied but typically include a progressive dementia, depression and "subcortical" dysfunction such as gait abnormalities, rigidity and neurogenic bladder. Treatment is largely supportive and includes a discussion about advanced directives, social support and antidepressant therapy. Control of hypertension and aspirin prophylaxis may help prevent further progression of white matter disease.(12)
C.8. Acquired immunodeficiency syndrome (AIDS)
AIDs is defined as Acquired immunodeficiency syndrome (AIDS) is defined as a condition of the progressive failure of the immune system caused by HIV, a lentivirus.Some researchers suggested that AIDS dementia complex (ADC) pathogenesis may be a multistep process that starts with HIV invasion of CNS by crossing the blood-brain barrier (BBB). It progresses by developing a chronic inflammatory status that can cause dysfunction in neurons and astrocytes that result in apoptotic death. Monocytes-macrophages (M/M) may play an important role by concealing the HIV transfer across the BBB. Furthermore, HIV-infected M/M could produce and release neurotoxic factors(13). Others showed that suggest a possible role for tumor necrosis factor-alpha in the development of neurological dysfunction. Increased levels of tumor necrosis factor-alpha messenger RNA were not associated with increased levels of IL-1 beta messenger RNA, suggesting differential regulation of these monokines in acquired immunodeficiency syndrome(14).
C.9. Creutzfeldt-Jakob disease (CJD)
Creutzfeldt-Jakob disease (CJD) is defined as a form of incurable and invariably fatal, degenerative neurological disorder that leads to a rapid decrease of mental function and movement as a result of infectious protein called a prion of which can replicate by converting their properly folded counterparts. According to the study of University of Gdańsk, in a report of a female, right-handed, age 68 adiagnosed with the Heidenhain variant of Creutzfeldt-Jakob Disease (HvCJD), over the crucial 6-week period the patient went from "Mild Cognitive Impairment" to a status resembling the final stages of Alzheimer's disease, without any evidence of a CVA, The only aspect of this case that does not fit the usual criteria for the Heidenhain variant is the fact that the patient survived over a year in a persistent vegetative state. Ophthalmologists and family physicians should be aware of the possibility of HvCJD in any patient over 60 presenting with otherwise inexplicable visual disturbances in the absence of significant ocular pathology, even when other symptoms of dementia may not be immediately noticeable(15).
C.10. Parkinson's disease
Parkinson's disease is defined as condition of a degenerative disorder of the central nervous system that leads to shaking (tremors) and difficulty with walking, movement, etc. with dementia commonly occurring in the advanced stages of the disease. Scales for Outcomes in Parkinson's Disease Motor and Psychiatric complications, MiniMental State Examination, Clinical Impression of Severity Index, and the Zarit Caregiver Burden Inventory. Patients in all stages of disease were included and 18.38 % were demented. The SEND-PD was responded by patients (86.16 %), caregivers (13.15 %), or both (0.69 %). Three factors (accounting for 66.63 % of the variance) were identified and considered as subscales: Psychotic symptoms, Mood/Apathy, and Impulse control disorders(16)
C.11. Huntington's disease
Huntington's disease is defned as condition of a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems(17). In the investigation to identify cognitive deficits that contribute to functional impairment to support dementia criteria that reflect HD neuropathology. Functional impairment was defined as 80 or below on the FIS. Speed of processing, initiation, and attention measures accounted for 70.0% of the variance in FIS ratings (linear regression) and correctly classified 91.7% of subjects as functionally impaired or intact (logistic regression). A definition of HD dementia that includes cognitive impairment in at least two areas of cognition but does not require a memory deficit, in the context of impaired functional abilities and a deteriorating course, more accurately reflects HD neuropathology and could lead to improved research methods and patient care.(17)
C.12. Motor Neurone disease (MND)
Motor neuron diseases are defined as a group of neurological disorders that affect the motor neurones, located in the central nervous system (or CNS). MND is a multisystem disorder associated with cognitive and behavioural changes which in some instances reaches the criteria for FTD, while a proportion of patients with FTD develop frank MND (18)
C.13. Multiple Sclerosis
is defined as condition of an inflammatory diseasethat cause the damage of the fatty myelin sheaths around the axons of the brain and spinal cord, leading to progressive interference with functions that are controlled by the nervous system such as vision, speech, walking, writing, and memory. there is a report that report that a female patient with severe cognitive presentation at the onset of MS, with dramatically demented evolution, and show MRI examination results. We discuss the published reports of primary cognitive types of MS.(19)
C.14. Obesity
Midlife and late-life obesity my increase the risk of dementia. In 480 persons with incident dementia, 245 with Alzheimer disease (no vascular dementia), and 213 with vascular dementia (with or without Alzheimer disease). In evaluations of midlife obesity, an increased risk of dementia was found for obese (BMI >30) vs normal-weight (BMI 20-25) persons, adjusted for demographics (hazard ratio [HR], 1.39; 95% confidence interval [CI], 1.03-1.87) and for cardiovascular risk factors (1.36; 0.94-1.95). The risk estimates were reversed in assessments of late-life BMI. Underweight persons (BMI <20) had an increased risk of dementia (1.62; 1.02-2.64), whereas being overweight (BMI >25-30) was not associated (0.92; 0.72-1.18) and being obese reduced the risk of dementia (0.63; 0.44-0.91) compared with those with normal BMI.(20)
C. 15. Etc.
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/19782001
(2) http://en.wikipedia.org/wiki/Lewy_body
(3) http://www.ncbi.nlm.nih.gov/pubmed/20513818
(4) http://www.ncbi.nlm.nih.gov/pubmed/16227556
(5) http://www.ncbi.nlm.nih.gov/pubmed/19748373
(6) http://www.ncbi.nlm.nih.gov/pubmed/22519566
(7) http://www.ncbi.nlm.nih.gov/pubmed/16401739
(8) http://www.ncbi.nlm.nih.gov/pubmed/22507301
(9) http://www.ncbi.nlm.nih.gov/pubmed/22496200
(10) http://www.ncbi.nlm.nih.gov/pubmed/20646296
(11) http://www.ncbi.nlm.nih.gov/pubmed/7604429
(12) http://www.ncbi.nlm.nih.gov/pubmed/9861880
(13) http://www.ncbi.nlm.nih.gov/pubmed/16540457
(14) http://www.ncbi.nlm.nih.gov/pubmed/8498837
(15) http://www.ncbi.nlm.nih.gov/pubmed/17179914
(16) http://www.ncbi.nlm.nih.gov/pubmed/22527230
(17) http://en.wikipedia.org/wiki/Huntington%27s_disease
(18) http://www.ncbi.nlm.nih.gov/pubmed/20629124
(19) http://www.ncbi.nlm.nih.gov/pubmed/20031302
(20) http://www.ncbi.nlm.nih.gov/pubmed/19273752
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