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PubMed2006

Are frontotemporal lobar degeneration, progressive supranuclear palsy and corticobasal degeneration distinct diseases?

New findings relating to the clinical, genetic and molecular bases of neurodegenerative disorders have led to a shift away from traditional nomenclatures of clinical syndromes. Historically, frontotemporal lobar degeneration (FTLD), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) were classified on the basis of distinct clinical and pathological features. In recent years, however, advances in molecular and genetic research have led clinicians to suggest that the similar etiologies of the three disorders warrant their amalgamation into a single disorder with three subtypes. In this Review, we consider the utility and validity of combining FTLD, CBD and PSP. The earliest reports of these disorders demonstrate their distinctiveness, whereas recent findings challenge traditional nomenclatures by showing etiological overlap. For example, tau inclusions have been confirmed in patients with CBD and those with PSP, and in some patients with FTLD, implying that all three disorders are 'tauopathies'. Furthermore, most patients with progressive nonfluent aphasia, a subtype of FTLD, show PSP or CBD post-mortem. Even tau-related cases of FTLD, CBD and PSP are distinguishable on the basis of other criteria, however, and many FTLD cases do not show tau pathology. We argue, therefore, that FTLD, CBD and PSP should be considered as pathologically similar but distinct syndromes. New research criteria for CBD and PSP should note that progressive nonfluent aphasia is often a precursor of these conditions.

Animals↗
PubMed1957

Studies on tubercle bacillus-monocyte relationship. II. Induction of monocyte degeneration by bacteria and culture filtrate: specificity of serum and monocyte effects on resistance to degeneration.

Studies of virulent, attenuated, and avirulent strains of tubercle bacilli have demonstrated the proficiency of virulent strains to effect degeneration of normal monocytes cultivated in the presence of normal serum. Attenuated strains were less active in this respect, and avirulent bacilli failed to induce monocytic degeneration. Comparison of the effects of virulent H37Rv with O.T., P.P.D., and a culture filtrate of H37Rv revealed a similarity in action of H37Rv and its filtrate. The action of O.T. and P.P.D. differed from that of H37Rv in that the greatest effect of H37Rv was upon normal cells as opposed to the effect of O.T. and P.P.D. upon immune cells. Additionally, it was demonstrated that immune serum (anti-BCG) protected immune cells against H37Rv but not against O.T. or P.P.D. The protection of immune cells by heterologous antisera (anti-Salmonella and anti-ovalbumin) as well as by homologous antiserum (anti-BCG) against the degenerative effects of H37Rv indicated a non-specificity in action of serum factors. The ability of the monocytes of animals immunized with BCG and the failure of monocytes of animals immunized with Salmonella rutgers to withstand parasitization with H37Rv, when both types of monocytes were cultivated in immune (anti-BCG) serum, indicated a specificity of cellular resistance.

Animals↗
PubMed1997

Adenovirus-mediated gene transfer of ciliary neurotrophic factor can prevent photoreceptor degeneration in the retinal degeneration (rd) mouse.

Mutations in the beta-subunit of the cGMP phosphodiesterase gene (betaPDE) can cause photoreceptor degeneration leading to blindness in humans, dogs, and mice. Since intravitreal administration of trophic factors has been shown to reduce photoreceptor death in the Royal College of Surgeons rat and the light overexposure models of photoreceptor degeneration, we have tested the possibility of rescuing photoreceptors in the rd mouse using ciliary neurotrophic factor (CNTF). Following intravitreal injection of an adenoviral vector encoding a ngf/cntf fusion gene into one eye of rd/rd mice, many strong CNTF-immunoreactive profiles are detected in various cell types of the injected eyes. Semiquantitative analysis of the corresponding retinae reveals that the photoreceptor-containing layer (outer nuclear layer, or ONL) retains significantly more rows of photoreceptor nuclei than that of eyes treated with a control (LacZ) vector, or untreated, for at least 18 days after vector administration (the longest survival time analyzed). A smaller, but significant, protective effect was also seen 9 days after intravitreal injection of recombinant CNTF. Because apoptotic cell death has been shown to be the common terminal fate of photoreceptors in the rd mouse and many other animal models of retinitis pigmentosa, these results suggest the possibility that administration of neurotrophic factors may prove beneficial in reducing photoreceptor loss in multiple forms of retinitis pigmentosa.

Adenoviridae↗
PubMed1997

Apophysial joint degeneration, disc degeneration, and sagittal curve of the cervical spine. Can they be measured reliably on radiographs?

STUDY DESIGN: Interexaminer reliability study. OBJECTIVES: To determine the reliability of grading apophysial joint and disc degenerative changes and the reliability of measuring sagittal curves on lateral cervical spine radiographs. SUMMARY OF BACKGROUND DATA: Several authors have proposed that the presented of degenerative changes and the absence of lordosis in the cervical spine are indicators of poor recovery from neck injuries caused by motor vehicle collisions. The validity of those conclusions is questionable because the reliability of the methods used in their studies to measure the presence of degenerative changes and the absence of lordosis has not been determined. METHODS: Kellgren's classification system for apophysial joint and disc degeneration, as well as the pattern and magnitude of the sagittal curve on 30 lateral cervical spine radiographs were assessed independently by three examiners. RESULTS: Moderate reliability was demonstrated for classifying apophysial joint degeneration with an intraclass correlation coefficient of 0.45 (95% confidence interval, 0.09-0.71). Classifying degenerative disc disease had substantial reliability, with an intraclass correlation coefficient of 0.71 (95% confidence interval, 0.23-0.88). Measuring the magnitude of the sagittal curve from C2 to C7 had excellent interexaminer agreement, with an intraclass correlation coefficient of 0.96 (95% confidence interval, 0.88-0.98) and an interexaminer error of 8.3 degrees. CONCLUSIONS: The classification system for degenerative disc disease proposed by Kellgren et al and the method of measurement of sagittal curves from C2 to C7 demonstrated an acceptable level of reliability and can be used in outcomes research.

Analysis of Variance↗
PubMed1976

[Composition and variability of bases in degenerate and non-degenerate positions in codons of various types of mRNA].

Codon base frequencies have been studied in all published mRNA sequences of more than 50 codons. Bases are not "random" in any codon position. Variability in degenerate position III is of the same order as in the other two positions (non-degenerate). The base distribution in each codon position is significantly different from that in each other position. Position I has the most distinctive make up. Correlations demonstrate that in this ensemble of 1,265 codons positions I and II have the same type of composition as in the decoded mRNA for the average protein.

Base Sequence↗
PubMed2003

Japanese age-related macular degeneration trial: 1-year results of photodynamic therapy with verteporfin in Japanese patients with subfoveal choroidal neovascularization secondary to age-related macular degeneration.

PURPOSE: To determine the effect and safety of verteporfin therapy (Visudyne) in Japanese age-related macular degeneration (AMD) patients. DESIGN: Open-label, multicenter, prospective, noncontrolled study. METHODS: The setting was five university hospitals in Japan. The study population was patients at least 50 years old, with best-corrected visual acuity of 20/40 to 20/200 inclusive and fluorescein angiography documenting subfoveal, classic-containing choroidal neovascularization (CNV) secondary to AMD and a lesion of greatest linear dimension <or= 5400 microm. For the intervention, patients received verteporfin intravenously followed by light administration 15 minutes after the infusion start. Additional treatment was given every 3 months through month 9 if leakage from CNV was observed on angiogram. The main outcome measure was percentage of lesions with progression of classic CNV beyond the area of the baseline lesion. RESULTS: Sixty-four patients were enrolled at five centers, and 61 patients completed the study. The median number of treatments given during the trial was three. At the 12-month examination, 12 patients (19%; 95% confidence interval: 11%-31%) had progression of classic CNV whereas 32 (50%) and 49 (77%) patients had no leakage from classic or occult CNV, respectively. The median visual acuity score (approximate Snellen equivalent) from baseline to month 12 increased from 50.0 (20/100)-56.5 (20/80(+2)) letters. Fourteen patients (22%) had visual disturbances, including two patients (3%) with acute vision decrease considered as serious adverse events and one patient (2%) with infusion-related back pain. No photosensitivity reactions were reported. CONCLUSIONS: Verteporfin therapy for subfoveal CNV in these Japanese patients appeared to have a similar or better angiographic and vision effect as that observed in Caucasian patients, with the same safety profile, supporting its use in Japanese patients.

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PubMed2004

Verteporfin therapy of subfoveal choroidal neovascularization in age-related macular degeneration: meta-analysis of 2-year safety results in three randomized clinical trials: Treatment Of Age-Related Macular Degeneration With Photodynamic Therapy and Verteporfin In Photodynamic Therapy Study Report no. 4.

PURPOSE: We sought to evaluate the detailed safety profile of photodynamic therapy with verteporfin in patients with subfoveal choroidal neovascularization (CNV) caused by age-related macular degeneration (ARMD) from the combined analysis of three multicenter, double-masked, placebo-controlled, randomized 24-month clinical trials of similar design (TAP Investigation Studies A and B and the VIP ARMD Trial), and to clarify the adverse reaction information in the current verteporfin product prescription information approved in the United States. METHODS: Nine hundred forty-eight patients were randomly assigned to verteporfin or placebo. Treatment was administered as described in previous reports. All general entry criteria were similar, so systemic safety results were combined for this analysis. Entry criteria for CNV lesion composition and visual acuity in the two TAP Investigation trials was different from those used in the VIP ARMD trial, so ocular safety results for the treated eye were not combined. RESULTS: The percentage of patients who experienced at least one ocular or nonocular adverse event, regardless of relationship to therapy, was similar between the verteporfin and placebo groups (92.3 and 89.1%, respectively, P = 0.114). The overall incidence of study eye adverse events was not significantly different between verteporfin and placebo. The only clinically relevant ocular adverse events reported with higher incidence after verteporfin compared with placebo were visual disturbances (22.1 versus 15.5% in TAP [P = 0.054] and 41.7 and 22.8% in VIP [P < 0.001]). Acute severe visual acuity decrease (defined as a visual acuity letter score decrease of at least 20, equivalent to at least four-line decrease, within 7 days of therapy) occurred in 3 patients treated with verteporfin in the TAP Investigation (0.7%) and 11 in the VIP ARMD trial (4.9%). Systemic adverse events with increased incidence after verteporfin compared with placebo, most of which were transient and mild or moderate, were injection site reactions (13.1 versus 5.6%; P < 0.001), photosensitivity reactions (2.4 versus 0.3%; P = 0.016), and infusion-related back pain (2.4 versus 0%; P = 0.004). No clinically relevant difference was observed between the verteporfin and placebo groups in any other adverse event. CONCLUSION: In 948 ARMD patients, verteporfin therapy had an overall safety profile similar to that for placebo, with a few exceptions. Visual disturbances, including acute severe visual acuity decrease, did not affect the net vision outcome benefits associated with treatment that has been reported previously. This detailed safety profile of verteporfin therapy clarifies the adverse reaction information in the current verteporfin product prescription information.

Aged↗
PubMed2000

Hypertension, cardiovascular disease, and age-related macular degeneration. Age-Related Macular Degeneration Risk Factors Study Group.

OBJECTIVES: To describe a case-control study of risk factors for neovascular and non-neovascular age-related macular degeneration (AMD) and to present findings on associations with systemic hypertension and cardiovascular disease. METHODS: Participants with and without neovascular and non-neovascular AMD were recruited from 11 ophthalmology practices in the New York, NY, metropolitan area. Comprehensive data collection included (1) a standardized interview, (2) blood pressure measurements, and (3) blood samples. Cases and controls were classified from fundus photograph gradings. Polychotomous logistic regression analyses were used to evaluate associations. RESULTS: Classification of 1222 sets of available photographs resulted in the inclusion of a neovascular case group (n = 182), a non-neovascular case group (n = 227), and a control group (n = 235). Neovascular AMD was positively associated with diastolic blood pressure greater than 95 mm Hg (odds ratio [OR] = 4.4), self-reported use of potent antihypertensive medication (OR = 2.1), physician-reported history of hypertension (OR = 1.8), use of antihypertensive medication (OR = 2.5), combinations of self-reported and physician-reported data on hypertension and its treatment (OR = 1. 7), high-density lipoprotein level (OR = 2.3), and dietary cholesterol level (OR = 2.2). Non-neovascular AMD was unrelated to hypertension or cholesterol level. No associations were found between either AMD type and other definitions of hypertension or other cardiovascular disease. CONCLUSIONS: These findings suggest that neovascular AMD is associated with moderate to severe hypertension, particularly among patients receiving antihypertensive treatment. They also support the hypotheses that neovascular and non-neovascular AMD may have a different pathogenesis and that neovascular AMD and hypertensive disease may have a similar underlying systemic process.

Aged↗
PubMed1995

Neuromuscular degeneration (nmd): a mutation on mouse chromosome 19 that causes motor neuron degeneration.

Neuromuscular degeneration, nmd, is a spontaneous autosomal recessive mutation in the mouse producing progressive hindlimb impairment caused by spinal muscular atrophy. We used an intersubspecific intercross between B6.BKs-nmd2J/+ and Mus musculus castaneus (CAST/Ei) to map the nmd mutation to mouse Chromosome (Chr) 19 with the most likely gene order: nmd-(D19Sel2, Pygm)-Cntf-Pomc2-D19Mit16-Cyp2c-Got1. nmd maps near muscle deficient, mdf, and has a very similar clinical phenotype, but allele tests and histological differences suggest that nmd is a distinct mutation at a different locus. Although closely linked, nmd recombined with the candidate genes muscle glycogen phosphorylase, Pygm, and ciliary neurotrophic factor, Cntf.

Animals↗
PubMed1997

Low dose radiation for subfoveal choroidal neovascularization in age-related macular degeneration. A pilot study: radiotherapy for age-related macular degeneration.

The aim of our pilot study was to test the effect of low dose radiation on classic and occult subfoveal choroidal neovascularization (CNV) in age-related macular degeneration (AMD). The posterior pole of the afflicted eye of 12 patients was irradiated with 5 Gray (Gy), and that of 34 patients with 8 Gy. The radiotherapy was done by a linear accelerator (6 MV X-rays) during 4 consecutive days with daily doses of 1.25 Gy and 2 Gy respectively. At the time of treatment, and 6 weeks, 6 months and 1 year after, a simultaneous fluorescein and ICG angiography of both eyes were carried out, and the distance visual acuity was measured. In none of the cases were we able to note a reduction in the subfoveal membrane's size. With regards to the visual acuity, the evolution was slightly better than the spontaneous courses described in existing literature. Further prospective randomized studies with higher dose radiation are necessary in order to determine the significance of radiotherapy in the treatment of this pathology.

Aged↗
PubMed1986

Development and degeneration of retina in rds mutant mice: effects of light on the rate of degeneration in albino and pigmented homozygous and heterozygous mutant and normal mice.

The effect of light on the rate of visual cell loss in mice afflicted by the rds (retinal degeneration slow) gene was analyzed by comparing the changes in the thickness of the outer nuclear layer. Visual cell loss in the pigmented, homozygous mutant mice, maintained in cyclic light, is slightly slower than in the albino mutant mice. In the pigmented mutant mice, exposed to constant light, and in the albino mutant mice, reared in darkness, rate of cell loss is not significantly altered. In the albino animals exposed to constant light, the rate of cell loss is faster in the homozygous mutant than in the normal, and intermediate in the heterozygous mutant retina. The accelerated cell loss in the mutant retina progresses from the centre to the periphery, and affects the rods earlier than the cones. This resembles the photic lesion in the normal retina but is unlike the genetic lesion in the mutant retina which appears to progress from the periphery to the centre and affects both rods and cones. It is concluded that the visual cells in the retina of rds mutant mice are more vulnerable to photic damage than those in the retina of normal mice.

Albinism↗
PubMed1995

Trial to establish an animal model of paraneoplastic cerebellar degeneration with anti-Yo antibody. 2. Passive transfer of murine mononuclear cells activated with recombinant Yo protein to paraneoplastic cerebellar degeneration lymphocytes in severe combined immunodeficiency mice.

Passive transfer of serum IgG or mononuclear cells from peripheral blood of a patient with paraneoplastic cerebellar degeneration (PCD) to rodents was carried out in order to examine the role of anti-Purkinje cell antibody (anti-Yo antibody) present in serum and cerebrospinal fluid of PCD patients. After a single injection of IgG into mouse brain, it was taken up by Purkinje cells and remained there for more than 36 h without Purkinje cell loss. Injection of PCD IgG together with complement or lipopolysaccharide-activated human macrophages or rat mononuclear cells into rat ventricles did not cause Purkinje cell loss. We also studied passive transfer of the PCD patient's lymphocytes to mice with severe combined immunodeficiency (SCID). We constructed a recombinant Yo fusion protein that has the leucine-zipper protein (Yo protein), the common epitope for anti-Yo antibody for immunizing mice, and that resulted in production of significant amounts of anti-Yo antibody. Spleen cells from these Yo protein immunized mice were injected intravenously or intracerebrally into naive mice that subsequently showed no neurological symptoms or loss of Purkinje cells. We conclude that the anti-Yo antibody, either in combination with or without complement or activated mononuclear cells, cannot be the sole cause of Purkinje cell loss.

Adenocarcinoma↗
PubMed1999

A prospective, randomized, double-masked trial on radiation therapy for neovascular age-related macular degeneration (RAD Study). Radiation Therapy for Age-related Macular Degeneration.

OBJECTIVE: To determine the efficacy of external beam radiation therapy on choroidal neovascularization (CNV) secondary to age-related macular degeneration (ARMD). DESIGN: Multicenter, parallel, randomized, double-masked clinical trial performed at nine ophthalmic and radiotherapeutic centers. PARTICIPANTS: Two hundred five patients were randomly assigned either to treatment with 8 fractions of 2 Gy external beam irradiation (n = 101) or to control with 8 fractions of 0 Gy (sham treatment, n = 104). Both patients and ophthalmologists were masked with regard to applied treatment. Patients with subfoveal classic or occult CNV, visual acuity of 20/320 or greater on the Early Treatment Diabetic Retinopathy Study chart, lesion size of 6 disc areas or less, history of visual symptoms of 6 months or less, and absence of foveal hemorrhage were recruited. INTERVENTION: In the treatment group, external beam irradiation with 8 fractions of 2 Gy was performed, whereas in the control group, sham treatment with 8 fractions of 0 Gy was applied. MAIN OUTCOME MEASURES: Primary outcome measure was the difference in visual acuity between baseline and after 1 year of follow-up. RESULTS: One hundred eighty-three patients (89.3%) completed the 1-year follow-up. The mean reduction in visual acuity was 3.5 +/- 4.7 lines in 88 patients of the 8- x 2-Gy treatment group and 3.7 +/- 3.8 lines in 95 patients of the 8- x 0-Gy control group. This difference was not statistically significant (P = 0.53, Mann-Whitney U test). At 1 year, 51.1% of treated patients and 52.6% of control subjects lost three or more lines (P = 0.88). Visual acuity in the presence of classic CNV dropped by 3.7 +/- 4.4 lines in 33 patients of the treatment group versus 4.3 +/- 3.9 lines in 36 patients of the control group (P = 0.47). Visual acuity in 114 patients with occult CNV dropped by 3.4 +/- 4.9 in the treatment group (55 patients) versus 3.4 +/- 3.8 lines in the control group (59 patients) (P = 0.80). CONCLUSIONS: In this randomized study, radiation therapy at a dose of 16 Gy applied in 8 fractions of 2 Gy provided no benefit as a treatment for subfoveal CNV secondary to ARMD at 1 year.

Aged↗
PubMedDate not supplied

Induction of retinal degeneration in a crab by light and okadaic acid in vitro: comparison with the Drosophila light-dependent retinal degeneration mutant w rdgBKS222.

Retinae of the crab Leptograpsus which had been maintained on a 12-h light/12-h dark cycle were cultured in vitro and exposed to 1 microM okadaic acid (OKA) at 0.75 h before light onset. Control retinae were subjected to the same routine and sampled at the same times without OKA treatment. At the concentration used, OKA totally inhibits types 1 and 2A protein phosphatases, minimally inhibits type 2B, and does not affect type 2C. 1 microM OKA provoked a diminution of rhabdom diameter measured at the level of the photoreceptor nuclei in the dark, some ommatidial cartridges being stripped of rhabdomeral microvilli altogether. After 1-h illumination (225-320 lux), further reduction of rhabdom diameter was modest in control retinae but precipitate in those treated with OKA. After 2 h, control rhabdom diameters showed a further, not significant, decline, but OKA had induced a resynthesis of massive structures with the light-microscopic appearance of rhabdoms. Electron microscopy revealed that they were heterogeneous and of the following kinds: (1) a minority of rhabdoms with normally disposed but distorted microvilli; (2) rhabdoms in the throes of events that parody normal assembly; and (3) rhabdomal volumes occupied by saccular organelles or by pleats or ruffles of irregular architecture. The cytoplasm of all such receptors was packed with free and bound ribosomes and endomembranes. The sequence of events parallels that seen during light-induced degeneration of photoreceptors of the Drosophila mutant w rdgBKS222. Preliminary experiments show that a protein kinase activator SC-9 mimics many of these effects in the dark in the presence of 1 microM OKA. As a working hypothesis, it is proposed that light activates protein kinases via diacylglycerols generated by the phototransduction cascade, and that in both crab retinas challenged with OKA and retinas of rdg BKS222 activation of a nuclear regulatory protein by hyperphosphorylation provokes a runaway transcription whose selectivity and extent remain to be determined.

Animals↗
PubMed1999

Neurofibrillary degeneration in progressive supranuclear palsy and corticobasal degeneration: tau pathologies with exclusively "exon 10" isoforms.

Pathological tau proteins that constitute the basic matrix of neuronal inclusions observed in numerous neurodegenerative disorders are disease specific. This is mainly the consequence of the aggregation of specific sets of tau isoforms according to the diseases, i.e., six isoforms in Alzheimer's disease (AD) and exclusively the three tau isoforms lacking the corresponding sequence of exon 10 (E10-) in Pick's disease (PiD). By using antibodies specific to the different tau isoforms and one- and two-dimensional gel electrophoresis followed by western blots, we demonstrate herein a third group of neurodegenerative disorders characterized by intraneuronal inclusions exclusively constituted of tau isoforms containing the sequence corresponding to exon 10, progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). Together, tau isoforms with exon 10 clearly differentiate three groups of neurodegenerative diseases: AD, PiD, and PSP/CBD. For each group, the neuropathological and clinical phenotypes are most likely related to specific sets of tau isoforms expressed by the vulnerable neuronal populations. The recently described mutations of the tau gene responsible for familial frontotemporal dementias also support this hypothesis.

Alzheimer Disease↗
PubMed2001

Gene replacement therapy in the retinal degeneration slow (rds) mouse: the effect on retinal degeneration following partial transduction of the retina.

The retinal degeneration slow (rds or Prph2(Rd2/Rd2)) mouse, a model of recessive retinitis pigmentosa, lacks a functional gene encoding peripherin 2. This membrane glycoprotein is required for the formation of photoreceptor outer segment discs. The striking feature of the rds mouse is the complete failure to develop outer segments. We have previously examined the short-term effect of gene replacement therapy using an adeno-associated (AAV) vector and demonstrated induction of outer segments and improvement of photoreceptor function. Here we have extended our analysis and have demonstrated that the potential for ultrastructural improvement is dependent upon the age at which animals are treated, but the effect of a single injection on photoreceptor ultrastructure may be long-term. However, there was no significant effect on photoreceptor cell loss, irrespective of the date of administration, despite the improvements in morphology and function. Our investigation excluded procedure-related damage, vector toxicity and immune responses as major factors which might counteract the benefits of photoreceptor restoration, but suggested that transgene over-expression is of significance. These findings suggest that successful gene therapy in patients with photoreceptor defects may ultimately depend upon intervention in early stages of disease and upon accurate control of transgene expression.

Animals↗
PubMed2001

Microglial activation parallels system degeneration in progressive supranuclear palsy and corticobasal degeneration.

The role of microglia in progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) is unknown. To address this issue we examined 10 cases of PSP, 5 cases of CBD, and 4 normal controls. Microglial and tau burdens were determined with image analysis on brain sections that had been immunostained with monoclonal antibodies to HLA-DR and phospho-tau. We found that microglial activation was greater in PSP and CBD than normal controls, and that the microglial burden correlated with the tau burden in most areas. There were distinct patterns of microglial activation and tau pathology in PSP and CBD, with PSP showing more pathology in infratentorial structures and CBD showing more pathology in supratentorial structures. These results support the notion that PSP and CBD are distinct clinicopathologic entities. Microglial activation was not well correlated with tau pathology in the brainstem of PSP, which suggests that brainstem pathology in PSP is not exclusively due to tau pathology. While the results do not necessarily support a direct causal link between microglial activation and neurodegeneration in PSP or CBD, they nevertheless suggest that microglia play a role in disease pathogenesis.

Aged↗
PubMed1997

Smoking and neovascular form of age related macular degeneration in late middle aged males: findings from a case-control study in Japan. Research Committee on Chorioretinal Degenerations.

AIMS: The risk of smoking habits for developing the neovascular form of age related macular degeneration (neovascular form of AMD) were studied by a case-control study in Japan. METHODS: 56 male patients with the neovascular form of AMD and 82 healthy male controls, aged 50 to 69 years, were enrolled. A self administered questionnaire provided necessary information for the study subjects. Questions on smoking included whether the study subjects have ever smoked or not, and if smoked, depth of smoke inhalation, use of extra filter, age at starting smoking, average number of cigarettes smoked per day, and duration of smoking. When a smoker had stopped smoking, age at cessation was also recorded. Unconditional logistic analysis was adapted to calculate age adjusted odds ratios and their 95% confidence intervals (CIs) for smoking related factors. RESULTS: Age adjusted odds ratio of developing the neovascular form of AMD was 2.97 (95% CI 1.00-8.84) for current smokers and 2.09 (0.71-6.13) for ex smokers, compared with non-smokers. All smoking habit/smoking history related variables such as use of extra filter, smoke inhalation level, age at starting smoking, duration of smoking, and Brinkman index were found to be significantly related to an increased risk of the neovascular form of AMD. CONCLUSIONS: Suggested is the strong possibility that cigarette smoking enhances the neovascular form of AMD risk in late middle aged males, though the magnitude of risk by smoking variables might be overestimated, in part, because of health oriented controls.

Aged↗