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Alzheimer’s disease is the most common cause of dementia in old age. With no cure available, it is emerging as a growing cause of deaths worldwide. Scientists are focusing their attempts on developing diagnostic methods and treatments to prevent dementia.

Alzheimer’s disease it is the most common cause of dementia. It causes progressive brain damage, affects memory and ability to perform day-to-day activities.

More than 36 million people worldwide are suffering from this disease.

Multiple studies have investigated risk factors and causes of this pathology but till date there is no definite cure for this condition.

What happens to the brain in Alzheimer’s disease?

Studies on the brains of people with Alzheimer’s disease show the deposition of β-amyloid protein plaques in between the nerve cells, as well as formation of so-called neurofibrillary tangles made of tau proteins within the neurons of the brain. These protein deposits disrupt the cell to cell communication in the brain and cause neuronal degeneration resulting in dementia.

While amyloid deposition in the brain is entirely pathological, the tau proteins is normal cell component which assist the brain cell communication and transport of substances in and out of cells. The abnormal and excessive deposition of tau proteins in the form of tangles disrupts the transport mechanism and cause dementia. The deposits also stimulate the immune system and initiate inflammatory changes which set up a cascade of reactions leading to the degeneration of the brain cells.

These are the commonly accepted theories that explain the pathology of Alzheimer’s disease. However, the definite cause of the disorder is yet to be established. Studies demonstrate that many people with amyloid deposits in the brain do not show any cognitive impairment even in their old age. Thus it proves that the mere presence of amyloid proteins does not cause the learning and memory problems although all patients diagnosed with Alzheimer’s disease have these deposits in their brain. Some studies implicate the soluble oligomers (the smaller components of β-amyloids) that float freely in the brain fluid and not the amyloid plaques in the pathogenesis of of Alzheimer’s disease. Researchers speculate that these oligomers can be bound to the plaques and the plaques tie down the oligomers until certain level is reached. When this level is exceeded, oligomers are set free to float in the cerebrospinal fluid resulting in brain cell damage.

Why is it difficult to treat Alzheimer’s disease?

There is no specific test that can detect the presence of this condition. It is actually a diagnosis of exclusion. The slow and gradual course of the disease and its multifaceted presentation makes the diagnosis of Alzheimer’s disease difficult. When dementia is observed in a patient, the next step involves ruling out various causes of dementia to narrow down the diagnosis to Alzheimer’s disease. 

By the time the diagnosis of Alzheimer’s disease is confirmed, the patient would have undergone considerable and irreversible brain damage.

What treatment strategy is presently available for this disorder?

Currently available FDA-approved drugs aim to ease the symptoms and improve the quality of life in the patients with this debilitating disorder. Some herbal products and dietary supplements for controlling or preventing the disease are available on the market but they are not sufficiently studied and their safety and efficacy is still questionable. Though a lot of novel drugs to control the disease progression are now under clinical investigations, they are either in the early stages of development or do not perform up to the mark in the large scale trials. The main treatments at present time include support therapies provided by health care workers and care givers.

Recent Advances In Diagnosing, Treating and Controlling The Cognitive Decline

Though controlling the disease progression is considered very difficult, several studies suggest that one may reduce the risk of developing Alzheimer’s disease or delay its progress by reducing the risk of cardiovascular diseases, obesity and diabetes.  However, many risk factors for the Alzheimer’s (such as genetic variations and family history of disease) are out of control. 

Scientists say that as for now, any positive result from the attempts to control or prevent the disease can be expected only with early start of intervention, preferably before the onset of the disease.

It is now possible to identify who will develop the disease years before the onset of brain damage

A blood test which can predict the development of Alzheimer's disease in a person even before the onset of symptoms was devised recently. The researchers at Georgetown University in Washington DC detected the depletion of 10 major chemicals (lipids) that were associated with the development of cognitive impairment in the study sample. The researchers believe that the changes in the levels of these metabolites occur at least 2-3 years before the development of Alzheimer’s disease and hence this test, when approved, should serve as a very effective means of detecting patients prone to the development of this disorder.

Novel treatment modalities are currently being investigated

Several indirect studies have already proposed a beneficial effect of caffeine on Alzheimer’s disease.A recent research has experimentally tested this effect of caffeine. The scientists have obtained positive results in animal studies and the new class of drug, if passes further trials, would serve as a promising treatment modality for Alzheimer’s disease.

Studies are in progress to develop new therapeutic molecules by a method called molecular topology.

New drugs would prevent the formation and deposition of beta-amyloid proteins in the brain.

Molecular topology allows the development of compounds that can treat the disease through a multidimensional approach. The researchers suggest that through this technique new drugs that can target multiple pathologies of the disease can be developed.

While focusing on the detrimental effect of the tau proteins on neuronal transmission, scientists have also developed antibodies that specifically act against the tau oligomers that cause behavioral and cognitive impairment sparing the normal tau proteins. This research was done on animals and further trials will be needed for approval. These antibodies are proposed to serve as a passive immunization strategy for Alzheimer’s disease. Several other studies are being conducted worldwide to develop a definitive treatment modality for this disease.

Alzheimer’s disease is a challenge for both the affected patients and the people around them. Many current studies aim to develop the treatments for this disorder. However, it would take a long time to develop new concepts into real drugs. Till then, the support and assistance provided by the care givers, regular consultation with the medical care provider and the regular usage of prescribed medications would help in improving the quality of life of people affected by the disease.

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  • Grammas P, Martinez J, Sanchez A et al. A New Paradigm for the Treatment of Alzheimer's Disease: Targeting Vascular Activation. J Alzheimer’s Dis. 2014 Feb 6
  • Hardy J, Selkoe DJ. The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics. Science. 2002 July 19, 297(5580): 353-6
  • Goedert M, Jakes R, Crowther RA et al. The abnormal phosphorylation of tau protein at Ser-202 in Alzheimer disease recapitulates phosphorylation during development. PNAS. 1993 Jun 1, 90(11): 5066-70
  • Wenk GL. Neuropathologic Changes in Alzheimer’s Disease. J Clin Psychiatry. 2003, 64(s9): 7-10
  • Esparza TJ, Zhao H, Cirrito JR et al. Amyloid-beta Oligomerization in Alzheimer Dementia vs. High Pathology Controls. Ann Neurol. 2013 Jan, 73(1): 104-19
  • Middleton LE, Yaffe K. Promising Strategies for the Prevention of Dementia. Arch Neurol. 2009, 66(10): 1210-15
  • Mapstone M, Cheema AK, Fiadaca MS et al. Plasma phospholipids identify antecedent memory impairment in older adults. Nat Med. 2014 Apr, 20(4): 415-8
  • Maia L & De Mendonca A. Does caffeine intake protect from Alzheimer’s disease? European J Neurol. 2002 Jul 3, 9(4): 377-82
  • Arendash GW, Schleif W, Rezai-Zadeh K et al. Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain β-amyloid production. Neuroscience. 2006 Niv 3, 142(4): 941-52
  • Laurent C, Eddarkaoui S, Derisbourq M et al. Beneficial effects of caffeine in a transgenic model of Alzheimer’s Disease-like Tau pathology. Neurobiology of Aging. 2014 Mar 31
  • Wang J, Land D, Ono K et al. Molecular Topology as Novel Strategy for Discovery for Drugs with Aβ Lowering and Anti-Aggregation Dual Activities for Alzheimer’s Disease. Plos One. 2014 Mar 26
  • Castillo-Carranza DL, Sengupta U, Guerrero-Munoz MJ et al. Passive Immunization with Tau Oligomer Monoclonal Antibody Reverses Taupathy Phenotypes without Affecting Hyperphosphorylated Neurofibrillary Tangles. Neurobiology of Disease. 2014 Mar 19, 34(12): 4260-72.
  • Photo courtesy of geralt by Pixabay : pixabay.com/en/alzheimer-s-dementia-woman-old-age-63610/
  • Photo courtesy of Kunstakademiets Designskole by Flickr : www.flickr.com/photos/danmarksdesignskole/5474694962

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