Probiotics and its benefits

By Sarika Garg

Probiotics are live pathogens that are destined to furnish health benefits. The concept of ‘Probiotics’ was pioneered in the early 20^th century when the ‘father of probiotics’, Noble laureate Elie Metchnikoff, suggested that people’s health could be refined by the consumption of favorable microorganisms. The idea was sustained by scientists and with the continued efforts, the term ‘Probiotics’, meaning ‘for life’, eventually came into practice.

Major population considers bacteria, fungi and other microbes as deleterious. But little do they know that several microorganisms assist our bodies function perfectly. For instance, intestinal bacteria destroy disease causing microbes, produce vitamins and help in food digestion. Numerous microorganisms live in our bodies and in point of fact, outstrip the human cells by 10 to 1.   

Probiotics may carry various microorganisms but the most common are Lactobacillus and Bifidobacterium groups of bacteria. Strengths of probiotics have been found to be eulogized in health magazines as well as on various products. Live bacteria naturally occur in certain foods viz. fermented vegetables and live-cultured yoghurt. Probiotics are also available as dietary supplements and in the form of products viz. skin creams.

Intensive research has been carried out on probiotics and the studies revealed that it might help cure a variety of maladies, including:

1.      Lower cholesterol levels

A study suggested that Lactobacillus reuteri, a probiotics strain found in dairy and meats, lowered the LDL levels in participants by 12% compared to the placebo group. Probiotics are known to alter gut microbiome to lower triglyceride levels or increase HDL cholesterol.

2.      Cavities and tooth decay

Detrimental effects of acid production from sugar could not be better understood by a sweet tooth person. Probiotics recognition has provoked much inquisitiveness for their role in oral health. Studies have reported the colonization of probiotics in the mouth and their effect on bio-film keeping the pathogens away. High calcium content in probiotics possibly play role in demineralization of teeth.

3.      Diarrhea

Several studies suggested that consumption of probiotics can help against diarrhea. Saccharomyces boulardii (or S. boulardii) is a potent probiotic that can help perpetuate the natural flora in the intestines and thereby curing and preventing the disagreeable diarrhea.

4.      Atopic dermatitis

Atopic dermatitis, also known as eczema, is a chronic inflammatory skin disease that is known to affect nearly 20% of children. A large number of studies have investigated the potential efficacy of probiotics in the prevention and treatment of eczema. A study published reported that mothers’ consumption of probiotics two months prior to giving birth and during first two months of breastfeeding showed a significant reduction in the risk of developing skin inflammation in the 

babies.

Despite the fact that some probiotics have shown promising results in research studies, compelling scientific evidence is inadequate to support specific uses of probiotics for health conditions. None of the probiotics have been approved by U.S. Food and Drug Administration (FDA) for treating any health issue. While probiotics have a good safety record in individuals, the information on the long-term safety of probiotics is limited. 

Copyright © 2017 HS Counseling. All rights reserved. 

Top 10 Landmarks in the Neuroscience World

By Sarika Garg

Neuroscience is the science of the nervous system, the study of which involves numerous researchers and doctors from different disciplines, extending from molecular biology and psychology to anatomy, physiology and pharmacology.  The nervous system comprises of the brain, spinal cord and peripheral nerves. It is made up of billions of nerve cells, called neurons, and trillions of supporting cells, called glial cells. The human brain is one of the most splendid organs in the human body. Thinking, feeling, planning, movements, memory, etc., everything is developed and controlled by our brain (Link 1). Alongside the most magnificent functions, several mysteries are associated with it making it the most intricate structure in the universe.  Many astonishing facts have been unraveled due to the tremendous progress made in medical science and technology. In this scientific era, it will be interesting to know that how much of the human brain was known in an ancient era and how the significant events occurred thereafter. Literature reports divulge that ancient Egyptian civilization was the first to have described 48 cases of brain injuries around the year 1700 B.C. Despite this creation of first medical document ever in the history of mankind, ancient Egyptians believed the ‘heart’ as the most important and the ‘brain’, on the other hand, the most inconsequential organ of the human body (Link 2). Please find below some of the notable events in the neuroscience world which helped brain garner much substantial attention. 

Brain stated as the seat of intelligence (460-379 B.C.)

The argument of whether the heart or the brain was the seat of intelligence remained unconcluded until the end of the 5^th century B.C. It was Hippocrates, a Greek physician, whose work stated that the brain is involved with sensation and is the seat of intelligence. He is considered as the founder of medicine and is referred to as the ‘Father of Western Medicine’. His oft-quoted statements showed a clear association between the mind and the brain:

‘Men ought to know that from the brain, and from the brain alone, arise our pleasures, joys, laughter and jests, as well as our sorrows, pains, griefs and tears. Through it, in particular, we think, see, hear and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant… I hold that the brain is the most powerful organ of the human body… wherefore I assert that the brain is the interpreter of consciousness…’ (Hippocrates: On the sacred disease. Quoted by Prioreschi [1996]) (Link 3).

Lecture on the brain anatomical procedures (177 A.D.)

Galen, a Greek physician in the Roman Empire, delivered a lecture entitled ‘On the brain’ to the Roman medical students in the year 177. In his lecture, along with the directives for a systematic brain dissection of an ox brain, he scattered knowledge about the various parts of the brain. He is credited with the earliest descriptions and speculations about the pineal, a small gland in the middle of the head which produces a hormone, melatonin. Melatonin is known to influence sexual development and sleep-wake cycles. He was a clever spectator and recognized that the brain becomes smaller in old animals. While Hippocrates set down the cornerstone of Greek medicine, Galen further developed its postulate and carried medicine to its apex (Link 4).

The discovery of the cerebrospinal fluid (1536)

Until the 16^th century, on the basis of Hippocrates and Galen findings, “spiritus animalis” with its mental functions was thought to be located within the cerebral ventricles. It was believed that blood moves to all parts of the body and no theory hypothesized blood circulation. The blood enriched by animal spirits was thought to reach the body’s organs where it gave life. After reverberating through centuries, the idea of “spiritus animalis” backed off only after 18 years when a Venetian physician, Nicolo Massa, described a large amount of fluid within cerebral ventricles. In his work he mentioned that ventricles are always full or semi full of watery substance. He was the first to notice and report the existence of the intraventricular fluid intracranially while making an autopsy. .  Among several physicians and anatomists who have laid the foundations of identification of the cerebrospinal fluid’s presence, Nicola Massa is considered as the first person to have described the cerebrospinal fluid properly (Link 5). 

The theory of brain function (1823-1824)

Marie Jean Pierre Flourens, a French physician, was accepted as a pioneer of the experimental methods in neuroanatomy and of the modern theory of the brain functions. He postulated that the brain-specific parts control specific functions. He conducted several ablation and stimulation methods along with many experimental investigations on mammalian species, especially rabbits and pigeons. Cerebral cortex, cerebellum and brainstem were shown to be functioned as a whole and in concomitance with every other part. Animal’s muscular coordination and sense of equilibrium vanished on removal of the cerebellum. Cerebral hemispheres and medulla were linked with the cognitive functions and vital functions, respectively. Death of the animal was noticed on desolation of the medulla oblongata (Link 6). Taking into account his achievements, he is today recognized as the founder of the modern field theory of brain function (Link 7).   

The discovery of the neuron (1889)

It won’t be wrong to say that the neuroscience discipline did not exist until the 19^th century pioneers Cajal and Golgi struck the right chord. Early in 1839, the cell theory was asserted according to which all tissues in the body are composed of individual cells. Later, ‘every cell comes from another cell’ theory was postulated. However, due to the dearth of good histological method to stain nervous structures, brain tissue was not considered to comply with the cell theory. In 1873 Camillo Golgi, an Italian physician, published his work on the silver nitrate staining method. This method was referred to as Golgi method and successfully stained neurons and neuroglia cells making them visible against the transparent background.  In 1887, Santiago Ramón y Cajal, a Spanish pathologist and neuroscientist confirmed the usefulness of Golgi method by carrying out the systematic study of the nervous system. He drew his observations quite accurately where he showed that the terminal and collateral fibres in the grey matter remained free, establishing simple contacts with the neuronal cell body and the dendrites of other adjacent nerve cells instead of forming a diffuse network. All his discoveries showed him the way to formulate the neuronal doctrine, a concept that the individual cells constitute the nervous system. Both Golgi and Ramón y Cajal were jointly awarded a Nobel Prize in Physiology or Medicine in 1906 in recognition of their work on the structure of the nervous system (Link 8).

The development of brain mapping (1909)

In the history of neuroscience, there has not been a single example as persuasive as the cytoarchitectonic map of the human brain. Korbinian Brodmann, a German neurologist, published his study in 1909 where he describes the dissociation of the cerebral cortex into 43 areas. He labeled his human map of the cortical area by a number between 1 and 52. His map is devoid of areas with the numbers 12-16 and 48-51 which was explained by Brodmann as the areas unidentifiable in the human cortex but well developed in other mammalian species. He utilized Nissl substance (cresyl violet) staining to divulge the distinct areal borders within the cortical sheet. His approach concluded that a particular anatomical structure corresponds to a particular function. In the 21^st century, Brodmann’s map is still in use for localizing neuroimaging data obtained in the living human brain (Link 9). 

The discovery of neurotransmitters (1921)

Neurotransmitters are the chemicals that allow neurotransmission. They are released from one neuron at the synaptic cleft, where they are accepted by a receptor on the next neuron. Communication between the neurons is the foundation of brain function and is accomplished by the movement of neurotransmitters. In 1921, a German scientist Otto Loewi published his work on frogs describing the chemical transmission. He conducted several experiments to characterize the substance and concluded it to be Acetylcholine. He was awarded the Nobel Prize in 1936 for his contributions (Link 10).

The invention of electroencephalography (1929)

Electroencephalography (EEG) is an electrophysiological monitoring and recording of the electrical activity of the brain. Hans Berger, a German psychiatrist, recorded the first human electroencephalograms in 1924. He published his work in 1929 where he described EEG changes associated with attention and mental effort, and alterations in the EEG associated with cerebral injury. His basic observations were later confirmed by other scientists revealing the dramatic change in humans EEG patterns during a night’s sleep. This technique provided early insight into diagnoses of sleep disorders, epilepsy, brain tumours, strokes and encephalopathies and has since been improved upon by use of modern techniques such as MRI (Link 11).

The invention of the electron microscope (1931)

By the beginning of the 20^th century, with the advancement of science and technology scientists were able to analyse some structures inside the cell using light microscopes. However, the limited resolution of the microscopes restricted the detailed study of the structures inside the cells. In 1931, German scientists Max Knoll and Ernst Ruska conquered the barrier by building the electron microscope (Link 12). An electron microscopic study of the Axo-somatic and axo-dendritic synapses of the cerebral cortex and several other made significant contributions in the understanding of the nervous system (Link 13). It also won Ernst Ruska the Nobel Prize in physics in 1986. 

The discovery of optogenetics

This is the latest and most exciting development in the field of Neuroscience. So far it has been used to identify specific neurons and networks like those in the amygdala that contribute to fear conditioning, to stimulate spiral ganglion in deaf mice and restoring auditory activity. Optogenetics is the use of light sensitive proteins to monitor and control living neurons which first attracted wide attention in 2005 (Link 14). This technique was investigated by several researchers but ultimately Karl Deisseroth, Edward Boyden and Gero Miesenböck have been recognised as pioneers in this field (Link 15). The uses of this technique could range from curing Parkinson’s disease and epilepsy, restoring vision, to further understanding and mapping of the brain and the central nervous system.

Link 1: http://brain.mcmaster.ca/BrainBee/Neuroscience.Science.of.the.Brain.pdf           

Link 2: http://www.ibro1.info/Pub/Pub_Main_Display.asp?LC_Docs_ID=3199

Link 3: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3115284/

Link 4: https://books.google.ca/books?id=3OWU1wnOy84C&pg=PA42&lpg=PA42&dq=galen+directives+for+the+brain+dissection&source=bl&ots=-0cnYSA3Ex&sig=-7u0Z3VlBRtv95EjDC4h7gzH8FA&hl=en&sa=X&ved=0ahUKEwiBrPzjvPTQAhVJjlQKHVn4DsQQ6AEIHTAB#v=onepage&q=galen%20directives%20for%20the%20brain%20dissection&f=false

Link 5: https://www.hindawi.com/journals/ari/2013/596027/

Link 6: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2117745/#ref1

Link 7: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1034464/pdf/medhist00179-0052.pdf

Link 8: http://hobertlab.org/wp-content/uploads/2013/03/DeCarlos_2007.pdf

Link 9: http://ling.umd.edu/~ellenlau/courses/nacs642/Zilles_2010.pdf

Link 10: http://www.animalresearch.info/en/medical-advances/timeline/neurotransmission-demonstrated/

Link 11: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1738204/pdf/v074p00009.pdf

Link 12: https://books.google.ca/books?id=o-IFp53_1-IC&pg=PA131&lpg=PA131&dq=Max+Knoll+and+Ernst+Ruska+invent+the+electron+microscope&source=bl&ots=pVJYkkhFQh&sig=dWdV1EHypKt2QQ_KkZkyJtj0Id0&hl=en&sa=X&ved=0ahUKEwj_26Xqg_fQAhWpI8AKHSs6D8I4FBDoAQgxMAM#v=onepage&q=Max%20Knoll%20and%20Ernst%20Ruska%20invent%20the%20electron%20microscope&f=false

Link 13: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1244535/pdf/janat00446-0039.pdf

Link 14: http://www.nature.com/nbt/journal/v29/n10/full/nbt.2016.html

Link 15: http://www.photonics.com/Article.aspx?AID=57936

Copyright © 2017 HS Counseling. All rights reserved. 

Milk taste can be enhanced by new LED display lights

New LED lights are known to reduce the energy bills across the globe but little did we know that they also help milk taste fresh, sweet and rich.

Remember the freshly pasteurized milk our grandparent's used to receive at their doorstep? It used to be so yummy. But we don't fall the same way for the milk that has been exposed to conventional fluorescent lights. Milk is delicious and nutritious but its consumption has been decreasing for several decades. This concern made the researchers at Virginia Tech to find ways to protect the milk characteristics to help the industry and to provide consumers the better and rich product. 

Researchers on conducting a series of experiments found that new LED lights positioned in milk display cabinets does help milk retaining its fresh taste but packaging should also be taken into consideration to get the fresh milk taste. Riboflavin, one of the nutrients in milk, oxidizes on exposure to fluorescent lights. This oxidation reaction changes the milk taste as well as reduces the nutritional value of the milk. Therefore, opaque milk packaging will also help to deliver milk with fresh and rich taste. 

This new lighting research has given the impetus to researchers to explore other ways to protect the natural taste of milk.  

Estimation of Dissolved oxygen (DO) in a water sample

Dissolved oxygen content in a water sample is indicative of its quality. Amount of dissolved oxygen in the water of river, pond, etc., determines whether biological flora and fauna, other aquatic living organisms viz. fishes will survive in it or not. Dissolved oxygen is also determined in waste water/ industrial effluent since it is an index of its pollution. Although nowadays, more sensitive methods like electrodes are available, still titrimetric method is in common use.  It is generally defined as number of milli-litres of oxygen gas per litre of water (ml. L^-1).

Principle:

The estimation of dissolved oxygen is done using titrimetric method. In the alkaline condition, manganese sulfate gets converted into manganous hydroxide. The oxygen present in the liquid combines with manganous hydroxide and oxidizes manganese to tetravalent state, MnO(OH)₂, and this MnO(OH)₂ on acidification liberates iodine equivalent to that of oxygen fixed. The liberated iodine is titrated using standard sodium thiosulfate solution and starch as indicator.

Sodium thiosulfate upon reaction with iodine forms sodium tetrathionate and sodium iodide. Here, progress of the reaction is monitored by using starch as indicator since starch after binding iodine gives blue colored complex.

2Na₂S₂O₃ + I₂ ==== Na₂S₄O₆ + 2NaI 

Reagents:

Sodium thiosulfate (N/40): Weigh 6.20 gm of sodium thiosulfate (Na2S2O3.5H2O), dissolve in water and make the volume 1 litre.  

Manganous sulfate (48%): Weigh 48 gm of manganous sulfate and dissolve in 100 ml of water.

Potassium iodide (15%) in potassium hydroxide (KOH) (70%): Prepare 70% KOH by dissolving 70 gm of KOH in 100 ml of water. Thereafter, weigh 15 gm of potassium iodide and dissolve in 70% KOH and make the volume 100 ml using 70% KOH.

Starch indicator (1%): Weigh 1 gm of soluble starch, add water and dissolve by gentle heating. Make the volume 100 ml using water.

Sulfuric acid (36N): Use commercial analytical grade sulfuric acid of 36 normality.

Protocol:

1. Pipette known volume of the liquid sample in a 250 ml glass bottle avoiding bubbles.

2. Add 2 ml each of manganous sulfate and alkaline potassium iodide solution in succession right at the bottom of the bottle using separate pipets and thereafter replace the stopper.

3. Shake the bottle well and allow the brown precipitate formed to settle. This brown precipitate is of MnO(OH)₂.

4. Add 2 ml of concentrated sulfuric acid and shake well to dissolve the brown precipitate.

5. Titrate the liberated iodine against standard sodium thiosulfate using starch as an indicator. At the end point, blue color will disappear.

If we check the stoichiometry of the reactions, one mole of oxygen will be equivalent to 2 moles of iodine.

After calculating the number of moles of iodine produced, calculate the number of moles of oxygen present in the sample. The dissolved oxygen content is generally expressed as mg/100 ml sample.

Source:

‘Biochemical Tests: Principles and Protocols’, Viva Books Pvt Ltd, New Delhi, India, 2012.

Frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17)

By Sarika Garg

FTDP-17 is a group of familial neurodegenerative Tauopathies characterized by diverse but overlapping clinical and neuropathologic features. According to several reports on clinical and neuropathologic features of FTDP-17, three major clinical syndromes have been delineated. These syndromes are disinhibition-dementia-parkinsonism-amyotrophy complex (DDPAC), pallid-ponto-nigral degeneration (PPND), and familial multiple system tauopathy with presenile dementia (MSTD). The clinical characteristics of these FTDP-17 Tauopathies variably include memory and language impairments, behavioral and psychiatric abnormalities, extrapyramidal signs, and motor deficits. However, all FTDP-17 brains from affected patients share a common neuropathology characterized by abundant neuronal and to a lesser extent glial fibrillary lesions composed of hyperphosphorylated Tau proteins and are associated with a remarkable loss of neurons in affected regions. 

Autosomal dominant inheritance of these FTDP-17 syndromes suggested that one or more genetic mutations might be pathogenic for these disorders, and linkage analyses showed co-segregation of disease with a genetic locus on chromosome 17q21.1. Since pathologic hallmarks of these disorders are Tau lesions and Tau gene resides within the disease locus of chromosome 17, Tau gene is an obvious candidate for pathogenic mutations in FTDP-17 kindreds. More than 40 different mutations in Tau gene are known to occur in FTDP-17.

Fig.: Tau mutations that result in frontotemporal dementia and parkinsonism linked to chromosome-17 (FTDP-17) map primarily to exons 9-12 or to the intronic region between exons 10 and 11.

In FTDP-17, two mechanisms have been proposed to mediate the effects of mutations in Tau gene. The first mechanism involves perturbations of the alternative splicing of exon 10 resulting change in the ratio of 4R:3R Tau. These mutations comprise a mixture of coding changes, within exon 10 (N279K, delK280, L284L, N296N/H, delN296, P301L/S, G303V, and S305S/N) and also intronic mutations close to the 5’ splice site of exon 10 (at positions +3, +11, +12, +13, +14, +16, +19, and +29). The second mechanism suggests that coding mutations (missense and deletions) directly cause deficits in the abilities of Tau to bind with microtubules (MTs) and promote assembly and stability of MTs. This has been linked to several Tau gene missense mutations including: G272V, delK280, P301L, P301S, V337M, G389R, and R406W using in vitro studies. Tau filaments formation is enhanced by heparin using recombinant G272V, P301L, V337M, and R406W mutant Tau proteins compared to wild type Tau protein. Moreover, mutations in exons other than those in exon 10 (V337M and R406W) promote Tau aggregation which is composed of all six isoforms, whereas other exon 10 mutations (P301L) increase 4R Tau in insoluble FTDP-17 brain fractions. Mutations in the intronic sequence adjacent to the stem loop structure in exon 10 have been identified that alter Tau splicing to increase soluble 3R Tau, leading to increased Tau proteolysis and neuronal apoptosis without deposition of insoluble Tau aggregates.

References:

Arrasate, M., Pérez, M., Armas-Portela, R., Avila, J., 1999. Polymerization of Tau peptides into fibrillar structures. The effect of FTDP-17 mutations. FEBS Lett. 446(1), 199-202.

Clark, L.N., Poorkaj, P., Wszolek, Z., Geschwind, D.H., Nasreddine, Z.S., Miller, B., Li, D., Payami, H., Awert, F., Markopoulou, K., Andreadis, A., D'Souza, I., Lee, V.M., Reed, L., Trojanowski, J.Q., Zhukareva, V., Bird, T., Schellenberg, G., Wilhelmsen, K.C., 1998. Pathogenic implications of mutations in the tau gene in pallido-ponto-nigral degeneration and related neurodegenerative disorders linked to chromosome 17. Proc Natl Acad Sci USA. 95(22), 13103-13107.

Foster, N.L., Wilhelmsen, K., Sima, A.A., Jones, M.Z., D'Amato, C.J., Gilman, S., 1997. Frontotemporal dementia and parkinsonism linked to chromosome 17: a consensus conference. Conference Participants. Ann Neurol. 41(6), 706-715.

Goedert, M., Spillantini, M.G. , 2001. Tau gene mutations and neurodegeneration. Biochem Soc Symp. 67, 59-71.

Hong, M., Zhukareva, V., Vogelsberg-Ragaglia, V., Wszolek, Z., Reed, L., Miller, B.I., Geschwind, D.H., Bird, T.D., McKeel, D., Goate, A., Morris, J.C., Wilhelmsen, K.C., Schellenberg, G.D., Trojanowski, J.Q., Lee, V.M., 1998. Mutation-specific functional impairments in distinct Tau isoforms of hereditary FTDP-17. Science. 282(5395), 1914-1917.

Lynch, T., Sano, M., Marder, K.S., Bell, K.L., Foster, N.L., Defendini, R.F., Sima, A.A., Keohane, C., Nygaard, T.G., Fahn, S., et al., 1994. Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex. Neurology. 44(10), 1878-1884.

Reed, L.A., Schmidt, M.L., Wszolek, Z.K., Balin, B.J., Soontornniyomkij, V., Lee, V.M., Trojanowski, J.Q., Schelper, R.L., 1998. The neuropathology of a chromosome 17-linked autosomal dominant parkinsonism and dementia ("pallido-ponto-nigral degeneration"). J Neuropathol Exp Neurol. 57(6), 588-601.

Schneider, A., Mandelkow, E., 2008. Tau-based treatment strategies in neurodegenerative diseases. Neurotherapeutics. 5, 443-457.

Spillantini, M.G., Goedert, M., Crowther, R.A., Murrell, J.R., Farlow, M.R., Ghetti, B., 1997. Familial multiple system Tauopathy with presenile dementia: a disease with abundant neuronal and glial Tau filaments. Proc Natl Acad Sci USA. 94(8), 4113-4118.

Stanford, P.M., Shepherd, C.E., Halliday, G.M., Brooks, W.S., Schofield, P.W., Brodaty, H., Martins, R.N., Kwok, J.B., Schofield, P.R., 2003. Mutations in the Tau gene that cause an increase in three repeat Tau and frontotemporal dementia. Brain. 126(Pt 4), 814-826.

Wijker, M., Wszolek, Z.K., Wolters, E.C., Rooimans, M.A., Pals, G., Pfeiffer, R.F., Lynch, T., Rodnitzky, R.L., Wilhelmsen, K.C., Arwert, F., 1996. Localization of the gene for rapidly progressive autosomal dominant parkinsonism and dementia with pallido-ponto-nigral degeneration to chromosome 17q21. Hum Mol Genet. 5(1), 151-154. 

Copyright © 2017 HS Counseling. All rights reserved. 

Alzheimer’s Disease

By Sarika Garg

Alzheimer’s disease (AD) is named after German psychiatrist and pathologist Dr. Alois Alzheimer. In 1907, he published an account of a 51-years old female patient, Auguste D from Frankfurt, who suffered from strong feelings of jealousy towards her husband, increased memory impairment, disorientation, hallucinations, and often loud and aggressive behaviour. After four and a half years of rapidly deteriorating mental illness, Auguste D died in a completely demented state. Postmortem histological analysis of her brain using the Bielschowsky silver technique revealed dense bundles of unusual fibrils within nerve cells (neurofibrillary tangles or NFTs) and numerous focal lesions within the cerebral cortex, subsequently named as ’’senile plaques’’.

Alzheimer’s disease is a devastating neurodegenerative disorder. It is an irreversible, progressive and fatal brain disease. It is neither infectious nor contagious, but it is the single most common form of dementia, a term used to describe a general decline in all areas of mental ability. The symptoms are deterioration in cognitive processes- memory, language, thinking and so on- with important repercussions on behaviour. About 50 per cent of the people with dementia suffer from Alzheimer’s disease, about 20 per cent from vascular dementia (caused by blockages in the supply of blood to the brain), and about 20 per cent from Lewy body dementia (characterized by tiny spherical deposits in the brain). The risk of getting Alzheimer’s disease increases as one gets older (beyond age 65). By age 85, about 35 out of 100 people have some form of dementia. Alzheimer’s disease is the ninth leading cause of death. It is estimated that more than 60 per cent of people with dementia live in developing countries, however, by 2040, it is expected to rise by 71 per cent.

Studies have supported the notion that 70 to 80% of the risk to develop Alzheimer’s disease is determined by genetic factors. Alzheimer’s disease is not a single-gene disorder. Genetically, Alzheimer’s disease (AD) is a complex and heterogeneous disease involving mutations and polymorphisms in multiple genes on several chromosomes. The two basic types of Alzheimer’s disease are: the late sporadic AD (SAD) and the early familial AD (FAD). The SAD represents the vast majority of cases whose aging itself is the unique important risk factor known. The apolipoprotein E (APOE) gene located on chromosome 19q13.2 has been confirmed unequivocally as a risk gene. Its ε4 allele increases the susceptibility to SAD whereas its ε2 allele confers protection against the late onset of AD. Besides cases arising sporadically, epidemiological studies indicate that about 30% of AD patients have a family history of disease and at least one first-degree relative is affected, however, only a few of them have a clear autosomal dominant inheritance. The FAD starts before 60 and accounts for less than 1% of the total number of AD cases. It is associated with gene mutations on chromosomes 1, 14, and 21. Only 5% of the amyloid precursor protein (APP) mutations have been estimated for FAD. Most of the FAD cases are caused by mutations in two genes namely presenelin 1 (PSEN1) and presenelin 2 (PSEN2). In AD, no mutation has been identified in the gene, MAPT which codes for Tau protein. However, more than 40 exonic and intronic mutations in MAPT present on chromosome 17q21.1, have been found in a familial dementia related to AD, and in the frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17).   

The actual causes of Alzheimer’s disease are not yet known with certainty. Alzheimer’s disease is not related to problems of the circulatory system. However, pathologically, Alzheimer’s disease is a progressive neurodegenerative disorder characterized by two main types of protein aggregation, intracellular neurofibrillary tangles (NFTs) and extracellular senile plaques (SPs). The NFTs consist of paired helical filaments (PHF) resulting from the hyper-phosphorylation of the microtubule-binding protein Tau. Senile plaques are principally composed of extracellular amyloid-ß (Aß) depositions. The amyloid cascade hypothesis posits that Aß triggers Tau pathology, but details of this relationship are poorly understood. However, there has been surprisingly scant attention focused on Tau as a therapeutic target. Advances in generating animal models with Tau pathology are helping to erase this deficit.

Fig.: Pathological hallmarks of Alzheimer’s disease. Extracellular plaques contain deposits of a protein fragment called ß-amyloid and tangles are twisted fibers of protein called Tau. Plaques build up between nerve cells and tangles form inside dying cells. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions. The plaques and tangles contribute to the degradation of the neurons in the brain and is a central feature associated with Alzheimer’s disease.

References:

http://www.ahaf.org/alzheimers/about/understanding/plaques-and-tangles.html

Alzheimer, A., Stelzmann, R.A., Schnitzlein, H.N., Murtagh, F.R., 1907. Uber eine eigenartige Erkankung der Hirnrinde. Allg Zschr f Psychiatr Psychisch-Gerichtl Mediz. 64, 146-148.

Beers, M. H., Jones, T. V., 2004. The Merck manual of health & aging. Whitehouse Station, NJ: Merck Research Laboratories.

Bertram, L., Tanzi, R.E., 2005. The genetic epidemiology of neurodegenerative disease. J Clin Invest. 115(6), 1449-1457.

Braak, H., Braak, E., 1997. Diagnostic criteria for neuropathologic assessment of Alzheimer’s disease. Neurobiol Aging. 18, S85-S88.

Delacourte, A., Sergeant, N., Champain, D., Wattez, A., Maurage, C.A., Lebert, F., Pasquier, F., David, J.P., 2002. Nonoverlapping but synergetic Tau and APP pathologies in sporadic Alzheimer's disease. Neurology. 59(3), 398-407.

Gatz, M., Pedersen, N.L., Berg, S., Johansson, B., Johansson, K., Mortimer, J.A., Posner, S.F., Viitanen, M., Winblad, B., Ahlbom, A., 1997. Heritability for Alzheimer's disease: the study of dementia in Swedish twins. J Gerontol A Biol Sci Med Sci. 52(2), M117-M125.

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Tips to be ahead of the pack in exams

Scoring high marks in the class doesn’t require one to study arduously or to become a dork. Some students study hard but still don’t manage to score higher than the mates who as a matter of fact haven’t burnt the midnight oil. On the day of grades’ announcement, a bunch of average scorers stare at a high scorer pal and whisper ‘lucky dude, he is a born intelligent’. However, unbeknownst to them ‘Geniuses are not always born – they can be made too’.

Research suggests that our brain is extraordinary malleable and it can be reformed in response to our lifestyle, physiology and environment. Reforming the brain concept is called as neuroplasticity. Similar to the DNA views, it was a myth that brain is static, but today we know that we have much more control over our body and brain than we thought. Brain has an astonishing ability to rewire itself in response to experience. Flexing grey matter can bring the best out of our brain cells. This can be achieved by lots of tips, changes to our way of living, selection of food and behavior. Some of them are as follows:

Smart drugs

Smart drugs are the supplements that are known to ameliorate cognitive function as well as overall brain health.  These drugs hold the promise of improving one’s ability to learn, consolidate memories, reasoning, judgement and concentration. Some drugs are already on the block and many others are on the move.  Apex GPA is one of the obtainable supplements and is composed of natural ingredients viz. Caffeine, Panax Ginseng and Ginkgo Biloba. It is certified by Health Canada and it appreciably improves memory, alertness and intellectual performances if tucked in as per the recommendation.

Physical training

Exercise has the ability to reduce insulin resistance, inflammation and stimulate the release of growth factors in the brain. This helps in the growth and survival of new brain cells. Exercise can also increase the blood flow to the whole body, including brain. This might help you recalling your memories down the line. Recommended workout session is at least 150 minutes a week of moderate aerobic activity or 75 minutes a week of vigorous aerobic activity. However, exam days are too occupied leaving almost no time and energy for workout; therefore, squeezing in short 10 minute walks per day is also beneficial. Happy walking!

Good sleep

When the exams are nearby, students often give up their sleep to have more time to study. But walking dead in the morning is not worth without a proper brain function. A growing body of scientific evidence suggests that having requisite sleep is certainly pivotal for proper brain function, concentration, response time and to stabilize your memories. Seven to nine hours of sleep per day for an adult is adequate. Sleep tight!

Although ‘Exams’ haunt majority of the students, it’s an integral component of every student’s life. The above mentioned tips along with the positive attitude and confidence will definitely go a long way in helping you overcome the exam fever. Good luck fellas!

Source: https://www.apexgpa.com/tips-to-be-ahead-of-the-pack-exams/

Good news for milk chocolate admirers!

We all know the fact that dark chocolate is healthier than the milk one. But still most of us like to have a sweeter one and not the bitter one. Our craving lets us forget that milk chocolate lacks most of the natural and healthy antioxidants as they are lost during the making process. But soon we may not have to worry about the nutrition value of our favorite milk chocolate, all thanks to our researchers. Researchers at North Carolina State University in Raleigh found that peanut skins can be used to give the milk chocolate the same nutritional benefits as the dark chocolate. Moreover, this secret ingredient won't have any affect on the mind blowing taste.

Best things happen by chance.

Researchers didn’t start their study with the aim of finding a secret ingredient for the milk chocolate. In the United States, most peanut skins are frittered away while peanuts are used in making peanut butter. They were interested in finding a way to make good use of the wasted peanut skins.

They planned to extract antioxidants from the peanut skins. An antioxidant is a substance that inhibits the oxidation of other molecules. Studies have shown that antioxidant rich foods have a low risk of heart disease. However, antioxidants may impart a perceptible bitter taste to foods. Therefore, to disguise the bitter taste, they decided to mix the peanut skin extracts with the maltodextrin. Maltodextrin is a white powder made from corn, rice, potato starch or wheat and is used as a food additive.

Post the preparation of the antioxidant mixture, researchers added it to the milk chocolate. This addition brought the antioxidant levels in the milk chocolate equal to that of a dark chocolate without having hampered the taste of a candy.

This finding doesn’t indicate that one should turn chocolate into a staple food. Chocolate does contain fat and sugar and should not be consumed in large quantities. 

Reference:
L.L. Dean ​et​ ​al., 2016.​ ​Minimizing the negative flavor attributes and evaluating consumer acceptance of chocolate fortified with peanut skin extracts.​ ​​Journal of Food Science.​ ​​​81, ​S2824-S2830.