Status of Baby Friendly Hospital Initiative in Neonatal Units.

Neonatal unit is more vulnerable and critical ward than any others. To assure breastfeeding in neonatal unit is one of the ways to reduce child morbidity and mortality. Baby friendly hospital initiative is the best method in hospital setting to assure breastfeeding. This cross-sectional descriptive study was conducted from July 2014 to December 2014 to find out the Status of Baby Friendly Hospital Initiative (BFHI) in neonatal unit of different public hospitals. The study area was consisting of several tertiary level hospitals in Dhaka city. Study was done in those hospital where declared as Baby Friendly Hospital Initiative. Total 137 data was collected from care givers (70) and healthcare providers (67). From hospital data it was found that all children discharged for last month were exclusively breastfed. Written breastfeeding policy was present in all hospitals but out of 67 staffs only 28(41.48%) staffs received training which was not fulfillment of the requirement of Global Criteria of UNICEF/WHO (BFHI External Assessment and Reassessment). In step 5 only 21(31.34%) staffs show or offered help for breastfeeding. In step 6 and 9 there were 100% fulfill the requirements, no teats and pacifier was found, no use of foods or drinks except medications. Nurses were co-operative but due to lack of training and motivation they were not fully aware about the importance of breastfeeding.

Detection of tropical bovine theileriosis by polymerase chain reaction in cattle.

Tropical bovine theileriosis, a tick borne disease, caused by, Theileria annulata with marked clinical signs of pyrexia (102-105 °F), enlargement of lymphnodes etc., causes heavy economic losses in terms of high mortality and morbidity rates. Diagnosis of theileriosis is mainly based on clinical symptoms and microscopic examination of stained blood smears and lymph node biopsy smears but limitations of these methods against Theileria sp. limits the specificity. Hence, to overcome the limitations, the present study reports the detection of T. annulata in blood samples of cattle by polymerase chain reaction. The study was conducted on 155 cattle having typical clinical symptoms and blood smear after staining with Giemsa stain was examined for the presence of T. annulata in RBC. The Primer sequences were used as per d'Oliveira et al. The assay employs primers specific for the gene encoding the 30-kDa major merozoite surface antigen of T. annulata and the amplification of 721 bp was done. Out of the total 155 animals, 34 were positive for T. annulata by blood smear method whereas 134 samples were positive by PCR. So diagnosis of blood samples by PCR is found to be the most sensitive and specific methodology as compared to cytological blood smear examination. The sensitivity was 23.88 % and specificity was 90.47 % of blood smear method considering PCR as gold standard and it was found that PCR is more sensitive than the conventional method of examination.

Evaluation of a service intervention to improve awareness and uptake of bowel cancer screening in ethnically-diverse areas.

BACKGROUND: Uptake of bowel cancer screening is lowest in London, in populations of lower socio-economic status, and in particular ethnic or religious groups. METHODS: We report on the evaluation of two interventions to improve uptake in an area including populations of low socio-economic status and considerable ethnic diversity. The interventions were face-to-face health promotion on bowel cancer screening at invitees' general practice and health promotion delivered by telephone only. Nine large general practices in East London were chosen at random to offer face-to-face health promotion, and nine other large practices to offer telephone health promotion, with 24 practices of similar size as comparators. Data at practice level were analysed by Mann-Whitney-Wilcoxon tests and grouped-logistic regression. RESULTS: There were 2034 invitees in the telephone intervention practices, 1852 in the face-to-face intervention practices and 5227 in the comparison practices. Median gFOBt kit uptake in the target population (aged 59-70) was 46.7% in the telephone practices, 43.8% in the face-to-face practices and 39.1% in the comparison practices. Significant improvements in the odds of uptake were observed following telephone intervention in both males (OR=1.39, 95% CI=1.20-1.61, P<0.001) and females (OR=1.49, 95% CI=1.29-1.73, P<0.001), while the face-to-face intervention mainly impacted uptake in males (OR=1.23, 95% CI=1.10-1.36), P<0.001) but did not lead to a significant increase in females (OR=1.12, 95% CI=0.96-1.29, P=0.2). CONCLUSIONS: Personally delivered health promotion improved uptake of bowel cancer screening in areas of low socio-economic status and high ethnic diversity. The intervention by telephone appears to be the most effective method.

PUMA mediates ER stress-induced apoptosis in portal hypertensive gastropathy.

Mucosal apoptosis has been demonstrated to be an essential pathological feature in portal hypertensive gastropathy (PHG). p53-upregulated modulator of apoptosis (PUMA) was identified as a BH3-only Bcl-2 family protein that has an essential role in apoptosis induced by a variety of stimuli, including endoplasmic reticulum (ER) stress. However, whether PUMA is involved in mucosal apoptosis in PHG remains unclear, and whether PUMA induces PHG by mediating ER stress remains unknown. The aim of the study is to investigate whether PUMA is involved in PHG by mediating ER stress apoptotic signaling. To identify whether PUMA is involved in PHG by mediating ER stress, gastric mucosal injury and apoptosis were studied in both PHG patients and PHG animal models using PUMA knockout (PUMA-KO) and PUMA wild-type (PUMA-WT) mice. The induction of PUMA expression and ER stress signaling were investigated, and the mechanisms of PUMA-mediated apoptosis were analyzed. GES-1 and SGC7901 cell lines were used to further identify whether PUMA-mediated apoptosis was induced by ER stress in vitro. Epithelial apoptosis and PUMA were markedly induced in the gastric mucosa of PHG patients and mouse PHG models. ER stress had a potent role in the induction of PUMA and apoptosis in PHG models, and the apoptosis was obviously attenuated in PUMA-KO mice. Although the targeted deletion of PUMA did not affect ER stress, mitochondrial apoptotic signaling was downregulated in mice. Meanwhile, PUMA knockdown significantly ameliorated ER stress-induced mitochondria-dependent apoptosis in vitro. These results indicate that PUMA mediates ER stress-induced mucosal epithelial apoptosis through the mitochondrial apoptotic pathway in PHG, and that PUMA is a potentially therapeutic target for PHG.

Achieving Millennium Development Goals 4 and 5 in Bangladesh.

Bangladesh has made commendable progress in achieving Millennium Development Goals (MDGs) 4 and 5. Since 1990, there has been a remarkable reduction in maternal and child mortality, with an estimated 57% reduction in child mortality and 66% in maternal mortality. This review highlights that, whereas Bangladesh is on track for achieving MDG 4 and 5A, progress in universal access to reproductive health (5B) is not yet at the required pace to achieve the targets set for 2015. In addition, Bangladesh needs to further enhance activities to improve newborn health and promote skilled attendance at birth.

Approaches to improving breast screening uptake: evidence and experience from Tower Hamlets.

This paper reports on an innovative whole-systems approach to improving uptake of breast screening in Tower Hamlets, a deprived borough in the East End of London with a large minority ethnic population. The approach, developed by the public health team at NHS Tower Hamlets, draws on analysis of needs and existing literature about effective interventions to promote breast screening. Social marketing research led to a campaign targeted at Bangladeshi women, together with a range of initiatives to promote breast screening through primary care services and community outreach through local well-known organisations. The breast screening service itself was upgraded and a new service specification is being introduced from April 2009.

Hepatitis B viral infection with nephrotic syndrome treated with lamivudine.

A 04 years old boy with 02 months history of generalized oedema and scanty micturition was diagnosed as nephrotic syndrome with hepatitis B viral infection. He had evidence of active viral replication. After 01 month treatment with oral lamivudine, his urine became protein free and after 04 months, he had seroconversion from HBeAg+ve to HBeAg-ve. Lamivudine was continued for 01 year. He had no relapse after discontinuation of therapy and remained well after 36 months of completion of therapy. He had no evidence of active viral replication during this period, however HBsAg remained positive indication carrier state. As most children with HBV associated nephropathy have no evidence of chronic hepatitis, all such children must undergo HBV screening and for chronic liver disease if HBV screening is positive. As such children do not respond to prednisolone or other immunosuppresive therapy which might harm them, antiviral therapy should be considered. Lamivudine is a suitable alternative to IFN alpha owing to its low cost, ease of administration and fewer side effects.

Chromium in some herbal drugs.

The use and demand of herbal drug is increasing day by day in both developing and developed countries due to the growing recognition that these are natural products having no or little side effects and can easily be available at affordable prices. Sometimes these are the only source of health care available to poor people particularly in South East Asia where more than 80% population depend on herbal drugs for their health care needs. Thus the quality and safety of herbal products is very important in order to have desired therapeutic efficacy. But in today's polluted environment with increasing automobile consumption and industrialization, WHO is emphasizing emphatically that without heavy metal assessment the herbal drug should not be used. The concentration of heavy metals including Cr is increasing in the environment and many hazardous effects are caused in the inhabitants of that environment (Prasad and Hagemeyer, 1999; Nriagu and Pacyna, 1998). For example, in human beings, due to Cr numbers of disorders occur like damage to liver, kidney, respiratory and nerve tissues. Besides enhancing risk of human lung cancer due to automobile exhaust and even irritation of skin have also been reported by excess of Cr (Anonymous, 1998; Anonymous 1988). Therefore it is mandatory to assess the Cr concentration in herbal drugs before use. Although some work has been carried out by Rai et al., 2001 a, b; Fuh et al., 2003; Al Ajasa et al., 2004 and Ernst 2002 but it is not enough and lot of work is required in this field.

Camptomelic dysplasia with sex reversal.

Camptomelic dysplasia is a disorder of the newborn characterized by congenital bowing and angulation of long bones together with other skeletal and extraskeletal defects. The affected newborn had dysmorphic features with bowing of the legs and bilateral talipes equinovarus. Radiology showed marked anterior bowing of both tibia with disproportionately short fibula, anterolateral bowing of the femurs and wide pelvic outlet with small iliac wings. She had sex reversal with normal female genitalia and 46, XY karyotype. Camptomelic dysplasia is generally considered to be a lethal skeletal dysplasia and most patients die in the neonatal period due to severe respiratory distress. Survivors may have learning difficulties, developmental delay, conductive hearing loss, myopia and recurrent chest infections. Because of its high associated mortality, prenatal diagnosis of camptomelic dysplasia is mandatory. The birth of a child with skeletal dysplasia is an emotionally difficult experience for parents.

Evaluation of hospitalized infants and young children with bronchiolitis - a multi centre study.

Four hundred and twenty nine young children with bronchiolitis admitted consecutively in different hospitals of Bangladesh were evaluated. Three hundred and forty eight children studied for their putative risk factors, clinical profile, management and the outcome. Both cases and controls were examined for respiratory syncytial virus (RSV) antibody status. The diagnosis of bronchiolitis was made on the basis of first attack of wheeze in previously healthy children below two years of age. Detailed history including the possible risk factors, the management and daily follow-up on the ward and the outcome at discharge were documented through a structured questionnaire. Chest x-ray was done in each case to find out the radiological changes. Blood of 266 patients and 30 controls were studied for RSV IgM and IgG antibody by ELISA. There were 66% male and 34% female children. The median age of the children was 3.0 months and 82.7% were below 6 months of age. Most of the babies were born term (88%), with ABW (73%), by normal vaginal delivery (88%). Exclusive or predominant breast-feeding were given in 72% cases. The location of the patient was rural in 55% cases. Around half of the parents were illiterate or slightly educated (up to 5 years schooling) fathers 46.5% and mothers 56% and majority of the parents were poor (74%). In 52% cases the number of family members in one room were four or more. Half of the parents (52%) were smokes and there was atopy in 26.5% families. The clinical features of bronchiolitis were mostly cough (99%), respiratory distress (97%), feeding difficulty (93%) and fast breathing (96%) (median RR 68/min). Fever (1000F or more) was in only 33% cases, though parents complained in 90% cases. All children (100%) had wheeze and crackles in lungs in 96% cases. Liver could be palpable in 83% and spleen in 42% cases. Important radiological features were increased translucency (96%), increased interstitial markings (87%), hyperinflation (75%) and streaky densities (61%). In 69.6% cases TLC was 12,000 or less and only 15% with a neutrophil fraction greater than 60%. Children were positive for IgM antibody in 43.6% cases and both IgM and IgG in 5.3% cases. The main modalities of treatment were antibiotics (99%) (Ampicillin, 76%), oxygen therapy (83%), nebulised salbutamol (76%) and intravenous fluid (51%). The median duration of hospital stay was 4 days. Most of the children were discharged with improvement (96%) with 2% mortality. Not a single case was diagnosed as bronchiolitis in hospitals outside Dhaka. Cefrtiaxone (72.5%) and parenteral steroids (70.5%) were the mainstay of therapy there.

Pharmacological targets to inhibit Alzheimer neurofibrillary degeneration.

Neurofibrillary degeneration appears to be required for the clinical expression of Alzheimer disease (AD) and related tauopathies. Given the polyetiology of these diseases and the pivotal involvement of neurofibrillary degeneration in their pathogenesis, inhibition of this lesion offers a promising therapeutic target. Studies from our laboratories have shown that there is a protein phosphorylation/dephosphorylation imbalance and that the microtubule associated protein tau is abnormally hyperphosphorylated in the brain of patients with AD and in this form it is the major protein subunit of paired helical filaments/neurofibrillary tangles (PHF/NFT). The abnormal tau which is polymerized into PHF/NFT neither promotes or inhibits in vitro microtubule assembly. In contrast the cytosolic abnormally hyperphosphorylated tau from AD brain, the AD P-tau neither associates with tubulin nor promotes in vitro microtubule assembly but instead it sequesters normal tau, MAP1 and MAP2 and inhibits microtubule assembly. The AD P-tau readily self-assembles in vitro into tangles of PHF/straight filaments under physiological conditions of protein concentration, pH, ionic strength and reducing conditions and this self assembly requires the abnormal hyperphosphorylation of this protein. The activity of phosphoseryl/phosphothreonyl protein phosphatase (PP)-2A which regulates the phosphorylation of tau, is compromised in AD brain. Thus, modulation of the activities of protein phosphatase-2A and tau kinases and inhibition of the sequestration of normal MAPs by AD P-tau offer promising therapeutic opportunities to inhibit neurofibrillary degeneration and the diseases characterized by this lesion.

Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach.

Neurofibrillary degeneration is a key histopathological brain lesion of Alzheimer disease (AD) and related neurodegenerative disorders such as frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17), commonly referred to as tauopathies. Microtubule associated protein (MAP) tau, which is a major MAP of a normal mature neuron is abnormally hyperphosphorylated in tauopathies and is the major protein subunit of paired helical filaments (PHF)/straight filaments (SF) which accumulate in the soma (as neurofibrillary tangles) and dystrophic neurites (as neuropil threads and as dystrophic neurites surrounding the beta-amyloid core in neuritic plaques in AD) of the affected neurons. Unlike normal tau which stimulates assembly and stabilizes microtubules, the abnormally hyperphosphorylated tau inhibits assembly and disrupts microtubules. The abnormally hyperphosphorylated tau competes with tubulin/microtubules in associating with normal tau, MAP1 and MAP2. This sequestration of normal MAPs by the abnormal tau results in the breakdown of the microtubules. The association of the abnormal tau with normal tau and not with MAP1 or MAP2 results in the formation of tangles of tau filaments. All these toxic properties of the abnormally hyperphosphorylated tau are eliminated by its enzymatic dephosphorylation. Activities of phosphoseryl/phosphothreonyl protein phosphatases (PP)-2A and PP-1 which can dephosphorylate the abnormal tau to a normal-like state are compromised in AD brain. Dephosphorylation by PP-2A and PP-2B and to a lesser extent by PP-1 restores the normal microtubule assembly promoting activity in AD P-tau in vitro. Neurofibrillary tangles of PHF isolated from AD brain are also dissociated on in vitro dephosphorylation with PP-2A, and the tau released by this treatment can stimulate microtubule assembly. Thus, it appears that the abnormal hyperphosphorylation of tau leads to neurodegeneration through breakdown of the microtubule network and that the abnormal tau on association with normal tau forms neurofibrillary tangles of tau filaments i.e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion.

Behavioral and biochemical studies of dichloromethane fraction from the Areca catechu nut.

The dichloromethane fraction from Areca catechu was found to inhibit monoamine oxidase type A isolated from the rat brain with an IC50 of 665 +/- 65.1 microg/ml. Studies with pharmacological models of depression, i.e., forced swim and tail-suspension tests, indicated that it caused significant reduction in the immobility time similar to that of moclobemide (a selective inhibitor of MAO-A) without causing a significant change in motor performance. Alkaloids such as arecaidine, arecoline, and a few other constituents, reported to be present in Areca catechu were also tested, but none of them were found to inhibit MAO. Present study suggests that the dichloromethane fraction from A. catechu possesses antidepressant property via MAO-A inhibition.

Mechanisms of neurofibrillary degeneration and the formation of neurofibrillary tangles.

Alzheimer disease (AD) has polyetiology. Independent of the etiology the disease is characterized histopathologically by the intraneuronal accumulation of paired helical filaments (PHF), forming neurofibrillary tangles, neuropil threads and dystrophic neurites surrounding the extracellular deposits of beta-amyloid in plaques, the second major lesion. The clincal expression of AD correlates with the presence of neurofibrillary degeneration; beta-amyloid alone does not produce the disease clinically. Thus arresting neurofibrillary degeneration offers a promising key target for therapeutic intervention of AD. The major protein subunit of PHF is the microtubule-associated protein tau. Tau in AD brain, especially PHF, is abnormally hyperphosphorylated and glycosylated. With maturation, the tangles are increasingly ubiquitinated. Levels of tau and conjugated ubiquitin are elevated both in AD brain and CSF. The AD abnormally phosphorylated tau (AD P-tau) does not promote microtubule assembly, but on dephosphorylation its microtubule promoting activity is restored to approximately that of the normal tau. The AD P-tau competes with tubulin in binding to normal tau, MAP1 and MAP2 and inhibits their microtubule assembly promoting activities. Furthermore, the AD P-tau sequesters normal MAPs from microtubules. The association of AD P-tau with normal tau but not with MAP1 or MAP2 results in the formation of tangles of 3.3 +/- 0.5 mm filaments. Deglycosylation of Alzheimer neurofibrillary tangles with endoglycosidase F/N-glycosidase F untwists the PHF resulting in tangles of thin filaments similar to those formed by association between the AD P-tau and normal tau. Dephosphorylation or deglycosylation plus dephosphorylation but not deglycosylation alone restores the microtubule assembly promoting activity of tau. In vitro AD P-tau can be dephosphorylated by protein phosphatases PP-2B, PP-2A and PP-1 but not PP-2C and all the three tau phosphatases are present in brain neurons. Tau phosphatase activity is decreased by approximately 30% in AD brain. Inhibition of PP-2A and PP-1 activities in SY5Y neuroblastoma by 10 nM okadaic acid causes breakdown of microtubules and the degeneration of these cells. It is suggested (I) that a defect(s) in the protein phosphorylation/dephosphorylation system(s) leads to a hyperphosphorylation of tau, (ii) that this altered tau causes disassembly of microtubules and consequently a retrograde neuronal degeneration; (iii) a pharmacological approach to AD is to enhance the tau phosphatase activity; and (iv) that CSF tau and conjugated ubiquitin levels are promising markers of AD brain pathology.

Anti-depressant activities of Areca catechu fruit extract.

The hexane and aqueous fractions of Areca catechu (A. catechu) have demonstrated anti-depressant properties in screens used to detect such activity. Similar properties had previously been detected in the plant's aqueous ethanolic extract. The aqueous ethanolic extract (F(1)), and the hexane (F(2)) and aqueous (F(5)) fractions inhibit monoamine oxidase (MAO) in rat brain homogenates. The aqueous fraction seems to be the most potent inhibitor of MAO and its effect is similar to that of clorgyline (a specific MAO-A inhibitor). The extract and fractions from A. catechu, therefore, merit further research in the quest for new anti-depressants.

Guanosine triphosphate binding to beta-subunit of tubulin in Alzheimer's disease brain: role of microtubule-associated protein tau.

In Alzheimer's disease, paired helical filaments composed mainly of abnormally phosphorylated tau accumulate in certain selected neurons of the brain, and microtubules are rarely seen in the affected cells. In the present study, the binding of 32P-labeled 8-azidoguanosine triphosphate ([gamma-32P]8N3GTP), the photoaffinity analogue of GTP to the beta-subunit of tubulin in brain homogenates was found to be markedly lower in patients with Alzheimer's disease than in aged control human cases. No significant differences were observed in the levels of the alpha- and beta-subunits of tubulin between Alzheimer's disease and control brains obtained 2-7 h postmortem. In nine of 19 Alzheimer's disease and 11 of 12 control autopsied brains (2-7 h postmortem and stored at -75 degrees C) tubulin was isolated successfully from brain cytosol by in vitro polymerization induced with DEAE-dextran. The GTP binding was observed in the two cycled assembled microtubule preparations from all the normal control, and in eight of nine Alzheimer's disease cases. Alzheimer's disease microtubule preparations contained varying amounts of abnormally phosphorylated tau, whereas no abnormal tau was detected in the control brain preparations. Addition of bovine tau to bovine, normal human, and Alzheimer's disease brain tubulin preparations markedly increased GTP binding to the beta-subunit. An alkaline phosphatase-treated paired helical filament-enriched preparation increased by approximately twofold the GTP binding to bovine brain tubulin. GTP binding to tubulin prepared by phosphocellulose chromatography of two cycled microtubules from three Alzheimer's disease and three normal control brains, revealed insignificant differences between the two groups. These findings have suggested that (1) tau protein promotes the GTP binding to the beta-subunit of tubulin, and (2) the breakdown of the microtubule system in brains of patients with Alzheimer's disease might in part be due to the abnormal phosphorylation of tau which depresses the GTP binding.

Perinatal outcome in relation to mode of delivery in meconium stained amniotic fluid.

Meconium staining of the amniotic fluid is a common complication during labour. When facilities like electronic monitoring, foetal blood sampling are not available, it is difficult to decide whether labour should be allowed to continue or caesarean section should be done. Even when caesarean section is done, meconium aspiration syndrome (MAS) can still occur and considerable morbidity and mortality may result in the newborn. Amino infusion is being considered as useful in decreasing MAS and its sequelae. Before resorting to amino infusion, we decided to analyse the perinatal outcome in meconium stained liquor to compare whether early caesarean section offered any advantage. This is a retrospective study of 150 labours complicated by thick meconium stained liquor, during a 12 month period (1992-93).

Serum immunoglobulin profiles of septicemic versus healthy neonates.

We studied 125 clinically suspected septicemic neonates (Patient) aged from 1 to 28 days and 25 healthy neonates (control) of comparable age and sexes. Cultures of blood were done and serum immunoglobulins (IgG, IgA) were estimated in all the subjects. Blood cultures were found positive in 45 (36%) patients. Preterm patients showed significantly higher number of positive blood cultures as compared to term patients. The mean serum IgG level in patients was found significantly lower than that of the controls. The serum IgG levels were also found significantly lower in 75 preterm as compared to 50 term, and in 45 blood culture positive patients as compared to 80 blood culture negative patients. On the other hand, the mean serum IgM level in patients was found significantly higher as compared to controls. Similarly, serum IgM levels were found higher in preterm patients as compared to term patients and in blood culture positive patients as compared to blood culture negative patients. No significant difference of mean serum IgA level was found among the subjects. It is evident from our study, that blood culture positive patients were mostly preterm, in whom transplacental passage of IgG is insufficient and due to low IgG level, preterm baby cannot counteract bacterial invasion and as such, suffer from septicemia more frequently. Septicemic neonates as a rule showed higher level of serum IgM due to synthesis by themselves in primary response to infection.

Levels of normal and abnormally phosphorylated tau in different cellular and regional compartments of Alzheimer disease and control brains.

Microtubule associated protein tau is abnormally phosphorylated in Alzheimer disease (AD) brain. In the present study we investigated (i) whether tau is axonal or both axonal and somatodendritic, (ii) whether tau is a marker of Alzheimer neurofibrillary pathology, and (iii) whether the levels of tau in the cytosol (100,000 x g supernate) from AD brain are altered. Frozen autopsied tissue from 20 AD, 17 normal aged and 15 neurological control cases obtained 3-8 h postmortem were analyzed. Levels of normal, total, and abnormally phosphorylated tau were determined by a radioimmunoslot-blot assay using mAb Tau-1 as the primary antibody. Both frontal gray matter homogenate and cytosol from normal brains had 30-45% higher levels of normal tau than the corresponding fractions from the white matter. In AD frontal and temporal cortices, the total tau levels were 6- to 7-fold higher than in cerebellar cortex (P < 0.01 and P < 0.02). Furthermore, tau levels of cerebellar cortex, an area of the brain unaffected with Alzheimer neurofibrillary changes, were indistinguishable between AD and control groups. The levels of normal tau in cytosol from both frontal gray and white matters in AD were reduced by approximately 40% (P < 0.05). The levels of total tau in AD frontal and temporal cortex were 4- to 5-fold higher than in the corresponding tissue from control cases (P < 0.01) and this increase was in the form of abnormally phosphorylated tau. These studies suggest (i) that there is probably at least as much tau in the somatodendritic compartment as in the axonal compartment, (ii) that the abnormally phosphorylated tau is a biochemical marker of the neurofibrillary pathology in AD, and (iii) that the levels of normal tau are significantly reduced in the 100,000 x g brain supernate from AD cases.