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J.P. Morgan 34th Annual Healthcare Conference & Biotech Showcase™ January 11 – 15, 2016 in San Francisco

Posted in BioIT: BioInformatics, BioIT: BioInformatics, NGS, Clinical & Translational, Pharmaceutical R&D Informatics, Clinical Genomics, Cancer Informatics, Conference Coverage with Social Media, Genetics & Innovations in Treatment, Genetics & Pharmaceutical, Genome Biology, Genomic Testing: Methodology for Diagnosis, Global Partnering & Biotech Investment, Pharmaceutical Discovery, Pharmaceutical Drug Discovery, Pharmaceutical Industry Competitive Intelligence, Pharmaceutical R&D Informatics, Pharmaceutical R&D Investment, Venture Capital on January 7, 2016| Leave a Comment »

J.P. Morgan 34th Annual Healthcare Conference & Biotech Showcase™ January 11 – 15, 2016 in San Francisco

Reporter: Aviva Lev-Ari, PhD, RN

J.P. Morgan 34th Annual Healthcare Conference

When:

January 11, 2016 – January 14, 2016 (all-day)

Where:

San Francisco, CA, USA

Conference AGENDA

http://jpmorgan.metameetings.com/confbook/healthcare16/agenda.php 

 

UPDATED on 1/10/2016

The definitive guide to the J.P. Morgan Healthcare Conference

By MEGHANA KESHAVAN Jan 9, 2016 at 2:22 PM

Image SOURCE

[Image courtesy of Flickr user Ryan McDonald]

http://medcitynews.com/2016/01/the-definitive-guide-to-the-j-p-morgan-healthcare-conference/

 

MAJOR BioTech Conferences in San Francisco –

The CAPITAL of BioTech for 2nd week in January 2016

 

• Festival Start up Health

http://festival.startuphealth.com/

• Biotech Showcase 2016

http://www.ebdgroup.com/bts/media/about_conf.php

• JP Morgan HealthCare Conference

http://globalbiodefense.com/2015/12/28/jp_morgan_healthcare_2016/#sthash.IhPw1DcA.dpuf

AGENDA

#JPM16

http://jpmorgan.metameetings.com/confbook/healthcare16/agenda.php

• The 9th Annual OneMedForum, San Francisco 2016 – A Private Investment Conference for OneMed Research Clients

http://www.onemedconferences.com/

 

• RESI@JPM — Redefining Early Stage Investments – Life Science Nation (LSN)

http://www.resiconference.com/

 

Venture Valkyrie (and capitalist) Lisa Suennen rightly pointed out that JPM is typically a male-dominated affair, which is why she’s written “JP Morgan: Where the Boys are… And not the Girls.”

In a field where women hold many senior positions in actual US healthcare corporations, they are drowned out at this conference by the advancing horde of finance guys in red ties and the CEOs that love them.

http://medcitynews.com/2016/01/the-definitive-guide-to-the-j-p-morgan-healthcare-conference/?rf=1

Signal Podcast on STAT

By LUKE TIMMERMANandMEG TIRRELL

JANUARY 7, 2016

MOLLY FERGUSON FOR STAT

How biotech went from a risky investment to a booming Business

http://www.statnews.com/2016/01/07/signal-podcast-birth-of-biotech/

Listen to Episode 5: By LUKE TIMMERMANandMEG TIRRELL

https://soundcloud.com/stat-signal-podcast/episode-5-san-francisco-in-january-is-where-new-medicines-get-made

San Francisco 2016

Union Square: Maps & Resources by MacDougall Biomedical Communications.

http://macb.io/jpm2016/

Biotech Showcase™ 2016 Program Overview

Sunday, January 10, 2016
1:00–5:00 pm	Additional Program Biotech Showcase™ pre-event The art and tactics of getting your fund raise done This workshop is focused on delivering results and securing funding at All Levels: Boards, Angels, VCs, Corporate Partners and Other Sources of Funds, with four hours of intensive and interactive discussion, on-your-feet sessions, war stories and insights aimed at folks looking for financing. It is designed to accelerate your funding activities and eliminate unnecessary noise. Preregistration is required, more information can be found here.
3:00–6:00 pm	Level 4, Cyril Magnin Foyer All Biotech Showcase attendees are invited to pick up name badges prior to the beginning of the conference on Monday.

Monday, January 11, 2016
7:00 am	Level 4, Cyril Magnin Foyer Registration Opens and Continental Breakfast
8:00–8:55 am	Workshops [ + ]The age of virtual pharma: Challenges and solutions for investor directors and successful boards [ + ]Alzheimer’s disease: Has the tide turned?				8:00 am–6:00 pm One-to-one Meetings ►

Hilton Union Square
333 O’Farrell Street
Level 2, Ballroom

8:00–9:50 am

Regenerative Medicine and Advanced Therapies State of the Industry Briefing

[ + ]Introduction and industry update

[ + ]The 2016 sector forecast: Upcoming clinical data events

[ + ]The promise of Regenerative Medicine and Advanced Therapies in oncology

8:00 am–12:00 pm

Company Presentations ►

Private Biotech
Public Biotech

12:00–1:30 pm

Lunch Plenary

[ + ]The great pricing debate: Navigating through an industry sea change

1:45–5:30 pm

Company Presentations ►

Private Biotech
Public Biotech

Tuesday, January 12, 2016
7:00 am	Level 4, Cyril Magnin Foyer Registration Opens and Continental Breakfast
8:00–8:55 am	Workshops [ + ]Corporate venture: Pharma’s eye on the early stage [ + ]The Life Sciences Report 2016 small-cap watchlist [ + ]London and the UK: A global hub for life sciences and investment				8:00 am–6:00 pm One-to-one Meetings ►

Hilton Union Square
333 O’Farrell Street
Level 2, Ballroom

8:00–9:15 am

Medtech Showcase State of the Industry Report

[ + ]Medtech Showcase State of the Industry Report

8:00 am–12:00 pm

Company Presentations ►

Private Biotech
Public Biotech

12:00–1:30 pm

Lunch Plenary

[ + ]State of the industry: It’s different this time

1:45–5:30 pm

Company Presentations ►

Private Biotech
Public Biotech

4:30–5:30 pm

Medtech Showcase Workshop

[ + ]Advanced medical technology: What investors need to know

 

Wednesday, January 13, 2016
7:00 am	Level 4, Cyril Magnin Foyer Registration Opens and Continental Breakfast
8:00–8:55 am	Workshops [ + ]FDA 2016: New FDA Commissioner, PDUFA reauthorization process and biomarkers [ + ]Investing in the immuno-oncology revolution: Follow the T cells				8:00 am–5:00 pm One-to-one Meetings ►

Hilton Union Square
333 O’Farrell Street
Level 2, Ballroom

8:00–9:00 am

Digital Health Showcase State of the Industry Report

[ + ]At the intersection of technology and medicine

8:00 am–12:00 pm

Company Presentations ►

Private Biotech
Public Biotech

10:00–11:00 am

Digital Health Showcase Workshop

[ + ]Who’s investing in digital medicine?

11:00–11:45 am

[ + ]Fireside chat

11:45 am–12:15 pm

Digital Health Showcase Discussion

[ + ]Top 10 digital health trends: Implications for early to mid-stage biopharma

12:00–1:30 pm

Lunch Plenary

[ + ]Bubble trouble? Have the biotech bulls had their run?

1:00–1:45 pm

Digital Health Showcase Workshop

[ + ]The regulatory pathway: Is it getting clearer?

4:00–5:00 pm

Digital Health Showcase Workshop

[ + ]A look at big pharma’s interest in digital medicine

1:45–5:00 pm

Company Presentations ►

Private Biotech
Public Biotech

5:00–6:00 pm

Level 4, Cyril Magnin Foyer

Closing Reception

 

SOURCE

http://www.ebdgroup.com/bts/program/index.php

About Biotech Showcase™ 2016

Previous conferences ►

Biotech Showcase™ 2016
January 11–13, 2016, San Francisco

Biotech Showcase™ 2015 Highlights

• 232 company presentations
• 2,100 attendees
• 1,276 companies
• 37 countries represented
• 4,277 one-to-one meetings
• 14 workshops and panels

Photos of Biotech Showcase 2015 ►

Biotech Showcase™ is an investor and networking conference devoted to providing private and public biotechnology and life sciences companies with an opportunity to present to, and meet with, investors and potential strategics in one place during the course of one of the industry’s largest annual healthcare investor conferences. Investors and biopharmaceutical executives from around the world gather in San Francisco during this critical week which is widely viewed as setting the tone for the coming year.

Now in its eighth year, this rapidly growing conference features multiple tracks of presenting companies, plenary sessions, workshops, networking, and an opportunity to schedule one-to-one meetings.

Biotech Showcase delegates include investors in private and public companies, sector analysts, bankers and industry professionals, as well as biopharmaceutical and life science company executives.

Biotech Showcase is produced by Demy Colton Life Science Advisors and EBD Group. Both organizations have a long history of producing high quality programs that support the biotechnology and broader life sciences industry.

http://www.ebdgroup.com/bts/media/about_conf.php

Biotech Showcase™ 2016 Press Releases

VideosBlogTwitterPrevious Press ReleasesPhoto GalleryVirtual Press Office/
PR Newswire offerAbout the ConferenceAbout the ProducersPress Registration

http://www.ebdgroup.com/bts/media/index.php

Press Contacts

Erin Righetti
EBD Group
+1 760 692 5907
erighetti@ebdgroup.com

Andrew Mielach
Tiberend Strategic Advisors, Inc.
+1 212 375 2695
amielach@tiberend.com

J.P. Morgan 34th Annual Healthcare Conference

When:

January 11, 2016 – January 14, 2016 (all-day)

Where:

San Francisco, CA, USA

Conference AGENDA

http://jpmorgan.metameetings.com/confbook/healthcare16/agenda.php 

 

J.P. MORGAN HEALTHCARE CONFERENCE 2016 SURVIVAL GUIDE

 

Whether you’re a conference veteran or a rookie, we hope this light-hearted guide helps you survive the week of life science mayhem in San Fransisco. At Chempetitive Group, we have a deep passion for everything life science—its people, its processes and its promise for the future. As life science marketers, this passion takes us to the industry’s biggest events every year, including the J.P. Morgan Healthcare Conference and related conferences each January. Over the years, we’ve learned our way around San Francisco’s Union Square—places we like to frequent.

 

January 11-14 San Francisco RAMP UP

Over 12,000 attendees

Over 15,000 meetings

Over 1,500 companies presenting

http://www.ebdgroup.com/bts/presenters/prs_comps.php

Over 40 countries represented Projected value of this year’s deals: unlimited

Surviving the J.P. Morgan Healthcare Conference [Plus Insider’s Guide]

POSTED BY:

ERIK CLAUSEN

Each January, the J.P. Morgan Healthcare Conference – perhaps the life science industry’s largest and most frenzied conference of the year – reliably draws thousands of investors and executives across the healthcare sector to San Francisco’s Union Square neighborhood as hundreds of companies present their latest innovations and dreams in an attempt to pique the interest of venture capitalists and potential partners. In addition to J.P. Morgan, parallel events Biotech Showcase, OneMedForum and RESI Conference ensure that there is a high density of biotech brainpower and capital in the City by the Bay.

The conference week is a mix of long days of presentations and lively evenings of cocktail parties and networking events. With more than 50 networking receptions, days of sessions, and still a volume of work to manage while away from the office, you might need some guidance on where to take your client or potential partner for a meeting, where to refuel or caffeinate, or simply where to hide from the chaos. For these reasons, we decided to let you into our world by creating this simple guide to surviving the 2016 J.P. Morgan Healthcare Conference week.

Download it and, if you happen to find yourself in one of our favorite spots, let us know with a direct message on Twitter at @chempetitive. Safe travels, have fun, and get some deals done.

JP Morgan 2016 Healthcare Conference Participants

The following organizations have released announcements of their participation in the 34th Annual JP Morgan Healthcare Conference:

• Abbott
• AbbVie
• Acacia Pharma
• Acorda Therapeutics
• Affiris
• AMN Healthcare
• Apogenix
• Argenx
• Athenahealth, Inc.
• Baxalta
• Baxter International
• Bionomics
• BioNTech
• Boston Scientific
• Cantel Medical
• Catalent
• Cellectis
• CONMED Corporation
• Cooper Companies
• CureVac
• Diplomat Pharmacy
• Endo International
• Epigenomics
• Exact Sciences
• Genisphere
• Gilead
• Glaukos Corporation
• HealthEquity
• HealthSouth
• HeartWare International
• Henry Schein
• Hill-Rom Holdings
• Hologic
• Horizon Pharma
• Illumina
• ImmunoGen
• Imprivata
• INC Research
• Incyte
• Intersect ENT
• Johnson & Johnson
• Luminex
• Magellan Health
• Maxim Integrated
• Mallinckrodt
• McKesson Corporation
• Medtronic
• MiMedx Group
• Moderna Therapeutics
• Mylan
• NanoString Technologies
• NOVADAQ
• OptiNose
• Orexo
• Oxford Immunotec
• PacBio
• Pacira Pharmaceuticals
• PerkinElmer
• Phlexglobal
• ProNAi Therapeutics
• PTC Therapeutics
• Quest Diagnostics
• Quintiles
• Quotient Limited
• Radius Health
• Santhera Pharmaceuticals
• Sera Prognostics
• Shire
• Spectranetics
• Stern Investor Relations
• St. Jude Medical
• The Medicines Company
• Teledoc
• Teleflex
• Valence Health
• Veracyte Inc.
• Vocera
• Wright Medical Group N.V.
• Zealand
• ZELTIQ
• Zoetis

http://globalbiodefense.com/2015/12/28/jp_morgan_healthcare_2016/#sthash.IhPw1DcA.dpuf

SOURCE

http://chempetitive.com/chemunity/jp-morgan-healthcare-conference-san-francisco-2016

http://info.chempetitive.com/hubfs/jp-morgan-infographic.pdf?__hssc=206009548.1.1452199074195&__hstc=206009548.1433c7a0bae9903565d9225ff3a2e21a.1452199074194.1452199074194.1452199074194.1&hsCtaTracking=4f124550-2dd0-4834-b2e3-1bcf78ce32bc%7C8020c5d5-e8f4-4e7e-95df-a299dd5dffbc

 

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Retromer in neurological disorders

Posted in Alzheimer's Disease, Etiology, Neurodegenerative Diseases, Neurological Diseases, Neuroscience, Pharmaceutical Analytics, Pharmaceutical Drug Discovery, Pharmaceutical Industry Competitive Intelligence, Pharmaceutical R&D Investment, Proteins, Proteomics, tagged Alzheimers Disease, Endosomes, Molecular neuroscience, Parkinsons disease on November 28, 2015| Leave a Comment »

Retromer in neurological disorders

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

 

Retromer in Alzheimer disease, Parkinson disease and other neurological disorders.

Scott A. Small and Gregory A. Petsko
Nature Reviews Neuroscience 16; 126–132 (2015)      http://dx.doi.org:/10.1038/nrn3896

 

As discussed in the forum (see video here), there are many cellular pathways which are believed to be perturbed in Alzheimer’s Disease. Recent work has suggested that deficits in retromer complex function may underlie impairment of endosomal trafficking in neurons and may contribute to AD pathogenesis. This recent review illustrates the function of the retromer complex and discusses how its dysfunction may contribute to neurodegeneration.

By Tim Spencer on 24 Nov, 2015

 

Retromer is a protein assembly that has a central role in endosomal trafficking, and retromer dysfunction has been linked to a growing number of neurological disorders. First linked to Alzheimer disease, retromer dysfunction causes a range of pathophysiological consequences that have been shown to contribute to the core pathological features of the disease. Genetic studies have established that retromer dysfunction is also pathogenically linked to Parkinson disease, although the biological mechanisms that mediate this link are only now being elucidated. Most recently, studies have shown that retromer is a tractable target in drug discovery for these and other disorders of the nervous system.

 

Yeast has proved to be an informative model organism in cell biology and has provided early insight into much of the molecular machinery that mediates the intracellular transport of proteins^1,2. Indeed, the term ‘retromer’ was first introduced in a yeast study in 1998 (Ref. 3). In this study, retromer was referred to as a complex of proteins that was dedicated to transporting cargo in a retrograde direction, from the yeast endosome back to the Golgi.

By 2004, a handful of studies had identified the molecular⁴ and the functional^{5, 6} homologies of the mammalian retromer, and in 2005 retromer was linked to its first human disorder, Alzheimer disease (AD)⁷. At the time, the available evidence suggested that the mammalian retromer might match the simplicity of its yeast homologue. Since then, a dramatic and exponential rise in research focusing on retromer has led to more than 300 publications. These studies have revealed the complexity of the mammalian retromer and its functional diversity in endosomal transport, and have implicated retromer in a growing number of neurological disorders.

New evidence indicates that retromer is a ‘master conductor’ of endosomal sorting and trafficking⁸. Synaptic function heavily depends on endosomal trafficking, as it contributes to the presynaptic release of neurotransmitters and regulates receptor density in the postsynaptic membrane, a process that is crucial for neuronal plasticity⁹. Therefore, it is not surprising that a growing number of studies are showing that retromer has an important role in synaptic biology^{10, 11, 12, 13}. These observations may account for why the nervous system seems particularly sensitive to genetic and other defects in retromer. In this Progress article, we briefly review the molecular organization and the functional role of retromer, before discussing studies that have linked retromer dysfunction to several neurological diseases — notably, AD and Parkinson disease (PD).

 

The endosome is considered a hub for intracellular transport. From the endosome, transmembrane proteins can be actively sorted and trafficked to various intracellular sites via distinct transport routes (Fig. 1a). Studies have shown that the mammalian retromer mediates two of the three transport routes out of endosomes. First, retromer is involved in the retrieval of cargos from endosomes and in their delivery, in a retrograde direction, to the trans-Golgi network (TGN)^5,6. Retrograde transport has many cellular functions but, as we describe, it is particularly important for the normal delivery of hydrolases and proteases to the endosomal–lysosomal system. The second transport route in which retromer functions is the recycling of cargos from endosomes back to the cell surface^{14, 15} (Fig. 1a). It is this transport route that is particularly important for neurons, as it mediates the normal delivery of glutamate and other receptors to the plasma membrane during synaptic remodelling and plasticity^{10, 11, 12, 13}.

a | Retromer mediates two transport routes out of endosomes via tubules that extend out of endosomal membranes. The first is the retrograde pathway in which cargo is retrieved from the endosome and trafficked to the trans-Golgi network (TGN). The second is the recycling pathway in which cargo is trafficked back from the endosome to the cell surface. The degradation pathway, which is not mediated by retromer, involves the trafficking of cargo from endosomes to lysosomes for degradation. b | The retromer assembly of proteins can be organized into distinct functional modules, all of which work together as part of retromer’s transport role. The ‘cargo-recognition core’ is the central module of the retromer assembly and comprises a trimer of proteins, in which vacuolar protein sorting-associated protein 26 (VPS26) and VPS29 bind VPS35. The ‘tubulation’ module includes protein complexes that bind the cargo-recognition core and aid in the formation and stabilization of tubules that extend out of endosomes, directing the transport of cargos towards their final destinations. The ‘membrane-recruiting’ proteins recruit the cargo-recognition core to the endosomal membrane. The WAS protein family homologue (WASH) complex of proteins also binds the cargo-recognition core and is involved in endosomal ‘actin remodelling’ to form actin patches, which are important for directing cargos towards retromer’s transport pathways. Retromer cargos includes a range of receptors — which bind the cargo-recognition core — and their ligands. PtdIns3P, phosphatidylinositol-3-phosphate.

• Full size image (159 KB)
• Download PowerPoint slide (271 KB)

• Figures index
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As well as extending the endosomal transport routes, recent studies have considerably expanded the number of molecular constituents and what is known about the functional organization of the mammalian retromer. Following this expansion in knowledge of the molecular diversity and organizational complexity, retromer might be best described as a multimodular protein assembly. The protein or group of proteins that make up each module can vary, but each module is defined by its distinct function, and the modules work in unison in support of retromer’s transport role.

Two modules are considered central to the retromer assembly. First and foremost is a trimeric complex that functions as a ‘cargo-recognition core’, which selects and binds to the transmembrane proteins that need to be transported and that reside in endosomal membranes^{5, 6}. This trimeric core comprises vacuolar protein sorting-associated protein 26 (VPS26), VPS29 and VPS35; VPS35 functions as the core’s backbone to which the other two proteins bind¹⁶. VPS26 is the only member of the core that has been found to have two paralogues, VPS26a and VPS26b^17,18, and studies suggest that VPS26b might be differentially expressed in the brain^{19, 20}. Some studies suggest that VPS26a and VPS26b are functionally redundant²¹, whereas others suggest that they might form distinct cargo-recognition cores^{20, 22}.

The second central module of the retromer assembly is the ‘tubulation’ module, which is made up of proteins that work together in the formation and the stabilization of tubules that extend out of endosomes and that direct the transport of cargo towards its final destination (Fig. 1b). The proteins in this module, which directly binds the cargo-recognition core, are members of the subgroup of the sorting nexin (SNX) family that are characterized by the inclusion of a carboxy-terminal BIN–amphiphysin–RVS (BAR) domain²³. These members include SNX1, SNX2, SNX5 and SNX6 (Refs 24,25). As part of the tubulation module, these SNX-BAR proteins exist in different dimeric combinations, but typically SNX1 interacts with SNX5 or SNX6, and SNX2 interacts with SNX5 or SNX6 (Refs 26,27). The EPS15-homology domain 1 (EHD1) protein can be included in this module, as it is involved in stabilizing the tubules formed by the SNX-BAR proteins²⁸.

A third module of the retromer assembly functions to recruit the cargo-recognition core to endosomal membranes and to stabilize the core once it is there (Fig. 1b). Proteins that are part of this ‘membrane-recruiting’ module include SNX3 (Ref. 29), the RAS-related protein RAB7A^{30, 31,32} and TBC1 domain family member 5 (TBC1D5), which is a member of the TRE2–BUB2–CDC16 (TBC) family of RAB GTPase-activating proteins (GAPs)²⁸. In addition, the lipid phosphatidylinositol-3-phosphate (PtdIns3P), which is found on endosomal membranes, contributes to recruiting most of the retromer-related SNXs through their phox homology domains³³. Interestingly, another SNX with a phox homology domain, SNX27, was recently linked to retromer and its function^{15, 34}. SNX27 functions as an adaptor for binding to PDZ ligand-containing cargos that are destined for transport to the cell surface via the recycling pathway. Thus, according to the functional organization of the retromer assembly, SNX27 belongs to the module that engages in cargo recognition and selection.

Recent studies have identified a fourth module of the retromer assembly. The five proteins in this module — WAS protein family homologue 1 (WASH1), FAM21, strumpellin, coiled-coil domain-containing protein 53 (CCDC53) and KIAA1033 (also known as WASH complex subunit 7) — form the WASH complex and function as an ‘actin-remodelling’ module^{28, 35, 36} (Fig. 1b). Specifically, the WASH complex functions in the rapid polymerization of actin to create patches of actin filaments on endosomal membranes. The complex is recruited to endosomal membranes by binding VPS35 (Ref. 28), and together they divert cargo towards retromer transport pathways and away from the degradation pathway.

The cargos that are transported by retromer include the receptors that directly bind the cargo-recognition core and the ligands of these receptors that are co-transported with the receptors. The receptors that are transported by retromer that have so far been identified to be the most relevant to neurological diseases are the family of VPS10 domain-containing receptors (including sortilin-related receptor 1 (SORL1; also known as SORLA), sortilin, and SORCS1, SORCS2 and SORCS3)⁷; the cation-independent mannose-6-phosphate receptor (CIM6PR)^{6, 5}; glutamate receptors¹⁰; and phagocytic receptors that mediate the clearing function of microglia³⁷. The most disease-relevant ligand to be identified that is trafficked as retromer cargo is the β-amyloid precursor protein (APP)^{7, 38, 39, 40, 41}, which binds SORL1 and perhaps other VPS10 domain-containing receptors⁴² at the endosomal membrane.

Retromer dysfunction

Guided by retromer’s established function, and on the basis of empirical evidence, there are three well-defined pathophysiological consequences of retromer dysfunction that have proven to be relevant to AD and nervous system disorders. First, retromer dysfunction can cause cargos that typically transit rapidly through the endosome to reside in the endosome for longer than normal durations, such that they can be pathogenically processed into neurotoxic fragments (for example, APP, when stalled in the endosome, is more likely to be processed into amyloid-β, which is implicated in AD⁴³ (Fig. 2a)). Second, by reducing endosomal outflow via impairment of the recycling pathway, retromer dysfunction can lead to a reduction in the number of cell surface receptors that are important for brain health (for example, microglia phagocytic receptors³⁷ (Fig. 2b)).

Retromer dysfunction has three established pathophysiological consequences. In the examples shown, the left graphic represents a cell with normal retromer function and the right graphic represents a cell with a deficit in retromer function. a | Retromer dysfunction causes increased levels of cargo to reside in endosomes. For example, in primary neurons, retromer transports the β-amyloid precursor protein (APP) out of endosomes. Accordingly, retromer dysfunction increases APP levels in endosomes, leading to accelerated APP processing, resulting in an accumulation of neurotoxic fragments of APP (namely, β-carboxy-terminal fragment (βCTF) and amyloid-β) that are pathogenic in Alzheimer disease. b | Retromer dysfunction causes decreased cargo levels at the cell surface. For example, in microglia, retromer mediates the transport of phagocytic receptors to the cell surface and retromer dysfunction results in a decrease in the delivery of these receptors. Studies suggest that this cellular phenotype might have a pathogenic role in Alzheimer disease. c | Retromer dysfunction causes decreased delivery of proteases to the endosome. Retromer is required for the normal retrograde transport of the cation-independent mannose-6-phosphate receptor (CIM6PR) from the endosome back to the trans-Golgi network (TGN). It is in the TGN that this receptor binds cathepsin D and other proteases, and transports them to the endosome, to support the normal function of the endosomal–lysosomal system. By impairing the retrograde transport of the receptor, retromer dysfunction ultimately leads to reduced delivery of cathepsin D to this system. Cathepsin D deficiency has been shown to disrupt the endosomal–lysosomal system and to trigger tau pathology either within endosomes or secondarily in the cytosol.

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The third consequence (Fig. 2c) is a result of the established role that retromer has in the retrograde transport of receptors, such as CIM6PR^{5, 6} or sortilin⁴⁴, after these receptors transport proteases from the TGN to the endosome. Once at the endosome, the proteases disengage from the receptors, are released into endosomes and migrate to lysosomes. These proteases function in the endosomal–lysosomal system to degrade proteins, protein oligomers and aggregates⁴⁵. Retromer functions to transfer the ‘naked’ receptor from the endosome back to the TGN via the retrograde pathway^{5, 6}, allowing the receptors to continue in additional rounds of protease delivery. Accordingly, by reducing the normal retrograde transport of these receptors, retromer dysfunction has been shown to reduce the proper delivery of proteases to the endosomal–lysosomal system^5,6, which, as discussed below, is a pathophysiological state linked to several brain disorders.

Although requiring further validation, recent studies suggest that retromer dysfunction might be involved in two other mechanisms that have a role in neurological disease. One study suggested that retromer might be involved in trafficking the transmembrane protein autophagy-related protein 9A (ATG9A) to recycling endosomes, from where it can then be trafficked to autophagosome precursors — a trafficking step that is crucial in the formation and the function of autophagosomes⁴⁶. Autophagy is an important mechanism by which neurons clear neurotoxic aggregates that accumulate in numerous neurodegenerative diseases⁴⁷. A second study has suggested that retromer dysfunction might enhance the seeding and the cell-to-cell spread of intracellular neurotoxic aggregates⁴⁸, which have emerged as novel pathophysiological mechanisms that are relevant to AD⁴⁹, PD⁵⁰ and other neurodegenerative diseases.

Alzheimer disease

Retromer was first implicated in AD in a molecular profiling study that relied on functional imaging observations in patients and animal models to guide its molecular analysis⁷. Collectively, neuroimaging studies confirmed that the entorhinal cortex is the region of the hippocampal circuit that is affected first in AD, even in preclinical stages, and suggested that this effect was independent of ageing (as reviewed in Ref. 51). At the same time, neuroimaging studies identified a neighbouring hippocampal region, the dentate gyrus, that is relatively unaffected in AD⁵². Guided by this information, a study was carried out in which the two regions of the brain were harvested post mortem from patients with AD and from healthy individuals, intentionally covering a broad range of ages. A statistical analysis was applied to the determined molecular profiles of the regions that was designed to address the following question: among the thousands of profiled molecules, which are the ones that are differentially affected in the entorhinal cortex versus the dentate gyrus, in patients versus controls, but that are not affected by age? The final results led to the determination that the brains of patients with AD are deficient in two core retromer proteins — VPS26 and VPS35 (Ref. 7).

Little was known about the receptors of the neuronal retromer, so to understand how retromer deficiency might be mechanistically linked to AD, an analysis was carried out on the molecular data set that looked for transmembrane molecules for which expression levels correlated with VPS35 expression. The top ‘hit’ was the transcript encoding the transmembrane protein SORL1 (Ref. 43). As SORL1 belongs to the family of VPS10-containing receptors and as VPS10 is the main retromer receptor in yeast³, it was postulated that SORL1 and the family of other VPS10-containing proteins (sortillin, SORCS1, SORCS2 and SORCS3) might function as retromer receptors in neurons⁷. In addition, SORL1 had recently been reported to bind APP⁵³, so if SORL1 was assumed to be a receptor that is trafficked by retromer, then APP might be the cargo that is co-trafficked by retromer. This led to a model in which retromer traffics APP out of endosomes⁷, which are the organelles in which APP is most likely to be cleaved by βAPP-cleaving enzyme 1 (BACE1; also known as β-secretase 1)⁴³; this is the initial enzymatic step in the pathogenic processing of APP.

Subsequent studies were required to further establish the pathogenic link between retromer and AD, and to test the proposed model. The pathogenic link was further supported by human genetic studies. First, a genetic study investigating the association between AD, the genes encoding the components of the retromer cargo-recognition core and the family of VPS10-containing receptors found that variants of SORL1 increase the risk of developing AD³⁸. This finding was confirmed by numerous studies, including a recent large-scale AD genome-wide association study⁵⁴. Other genetic studies identified AD-associated variants in genes encoding proteins that are linked to nearly all modules of the retromer assembly⁵⁵, including genes encoding proteins of the retromer tubulation module (SNX1), genes encoding proteins of the retromer membrane-recruiting module (SNX3 and RAB7A) and genes encoding proteins of the retromer actin-remodelling module (KIAA1033). In addition, nearly all of the genes encoding the family of VPS10-containing retromer receptors have been found to have variants that associate with AD⁵⁶. Finally, a study found that brain regions that are differentially affected in AD are deficient in PtdIns3P, which is the phospholipid required for recruiting many sorting nexins to endosomal membranes⁵⁷. Thus, together with the observation that the brains of patients with AD are deficient in VPS26a and VPS35 (Refs 7,37), all modules in the retromer assembly are implicated in AD.

Studies in mice^{39, 58, 59}, flies³⁹ and cells in culture^{34, 40, 41, 60, 61} have investigated how retromer dysfunction leads to the pathogenic processing of APP. Although rare discrepancies have been observed among these studies⁶², when viewed in total, the most consistent findings are that retromer dysfunction causes increased pathogenic processing of APP by increasing the time that APP resides in endosomes. Moreover, these studies have confirmed that SORL1 and other VPS10-containing proteins function as APP receptors that mediate APP trafficking out of endosomes.

Retromer has unexpectedly been linked to microglial abnormalities³⁷ — another core feature of AD — which, on the basis of recent genetic findings, seem to have an upstream role in disease pathogenesis^{54, 63}. A recent study found that microglia harvested from the brains of individuals with AD are deficient in VPS35 and provided evidence suggesting that retromer’s recycling pathway regulates the normal delivery of various phagocytic receptors to the cell surface of microglia³⁷, including the phagocytic receptor triggering receptor expressed on myeloid cells 2 (TREM2) (Fig. 2b). Mutations in TREM2 have been linked to AD⁶³, and a recent study indicates that these mutations cause a reduction in its cell surface delivery and accelerate TREM2 degradation, which suggests that the mutations are linked to a recycling defect⁶⁴. While they are located at the microglial cell surface, these phagocytic receptors function in the clearance of extracellular proteins and other molecules from the extracellular space⁶⁵. Taken together, these recent studies suggest that defects in the retromer’s recycling pathway can, at least in part, account for the microglial defects observed in the disease.

The microtubule-associated protein tau is the key element of neurofibrillary tangles, which are the other hallmark histological features of AD. Although a firm link between retromer dysfunction and tau toxicity remains to be established, recent insight into tau biology suggests several plausible mechanisms that are worth considering. Tau is a cytosolic protein, but nonetheless, through mechanisms that are still undetermined, it is released into the extracellular space from where it gains access to neuronal endosomes via endocytosis^{66, 67}. In fact, recent studies suggest that the pathogenic processing of tau is triggered after it is endocytosed into neurons and while it resides in endosomes⁶⁷. Of note, it still remains unknown which specific tau processing step — its phosphorylation, cleavage or aggregation — is an obligate step towards tau-related neurotoxicity. Accordingly, if defects in microglia or in other phagocytic cells reduce their capacity to clear extracellular tau, this would accelerate tau endocytosis in neurons and its pathogenic processing.

A second possibility comes from the established role retromer has in the proper delivery of cathepsin D and other proteases to the endosomal–lysosomal system via CIM6PR or sortilin (Fig. 2c). Studies in sheep, mice and flies⁶⁸ have shown that cathepsin D deficiency can enhance tau toxicity and that this is mediated by a defective endosomal–lysosomal system⁶⁸. Whether this mechanism leads to abnormal processing of tau within endosomes or in the cytosol via caspase activation⁶⁸ remains unclear. As discussed above, retromer dysfunction will lead to a decrease in the normal delivery of cathepsin D to the endosome and will result in endosomal–lysosomal system defects. Retromer dysfunction can therefore be considered as a functional phenocopy of cathepsin D deficiency, which suggests a plausible link between retromer dysfunction and tau toxicity. Nevertheless, although these recent insights establish plausibility and support further investigation into the link between retromer and tau toxicity, whether this link exists and how it may be mediated remain open and outstanding questions.

Parkinson disease

The pathogenic link between retromer and PD is singular and straightforward: exome sequencing has identified autosomal-dominant mutations in VPS35 that cause late-onset PD^{69, 70}, one of a handful of genetic causes of late-onset disease. However, the precise mechanism by which these mutations cause the disease is less clear.

Among a group of recent studies, all^{46, 48, 71, 72, 73, 74, 75, 76} but one⁷⁷ strongly suggest that these mutations cause a loss of retromer function. At the molecular level, the mutations do not seem to disrupt mutant VPS35 from interacting normally with VPS26 and VPS29, and from forming the cargo-recognition core. Rather, two studies suggest that the mutations have a restricted effect on the retromer assembly but reduce the ability of VPS35 to associate with the WASH complex^{46, 75}. Studies disagree about the pathophysiological consequences of the mutations. Four studies suggest that the mutations affect the normal retrograde transport of CIM6PR^{71, 73, 75, 76} from the endosome back to the TGN (Fig. 2c). In this scenario, the normal delivery of cathepsin D to the endosomal–lysosomal system should be reduced and this has been empirically shown⁷³. Cathepsin D has been shown to be the dominant endosomal–lysosomal protease for the normal processing of α-synuclein⁷⁶, and mutations could therefore lead to abnormal α-synuclein processing and to the formation of α-synuclein aggregates, which are thought to have a key pathogenic role in PD.

A separate study suggested that the mutation might cause a mistrafficking of ATG9, and thereby, as discussed above, reduce the formation and the function of autophagosomes⁴⁶. Autophagosomes have also been implicated as an intracellular site in which α-synuclein aggregates are cleared. Thus, although future studies are needed to resolve these discrepant findings (which may in fact not be mutually exclusive), these studies are generally in agreement that retromer defects will probably increase the neurotoxic levels of α-synuclein aggregates⁴⁸.

Several studies in flies^{71, 74} and in rat neuronal cultures⁷¹ provide strong evidence that increasing retromer function by overexpressing VPS35 rescues the neurotoxic effects of the most common PD-causing mutations in leucine-rich repeat kinase 2 (LRRK2). Moreover, a separate study has shown that increasing retromer levels rescues the neurotoxic effect of α-synuclein aggregates in a mouse model⁴⁸. These findings have immediate therapeutic implications for drugs that increase VPS35 and retromer function, as discussed in the next section, but they also offer mechanistic insight. LRRK2 mutations were found to phenocopy the transport defects caused either by theVPS35 mutations or by knocking down VPS35 (Ref. 71). Together, this and other studies⁷⁸suggest that LRRK2 might have a role in retromer-dependent transport, but future studies are required to clarify this role.

Other neurological disorders

Besides AD and PD, in which a convergence of findings has established a strong pathogenic link, retromer is being implicated in an increasing number of other neurological disorders. Below, we briefly review three disorders for which the evidence of the involvement of retromer in their pathophysiology is currently the most compelling.

The first of these disorders is Down syndrome (DS), which is caused by an additional copy of chromosome 21. Given the hundreds of genes that are duplicated in DS, it has been difficult to identify which ones drive the intellectual impairments that characterize this condition. A recent elegant study provides strong evidence that a deficiency in the retromer cargo-selection protein SNX27 might be a primary driver for some of these impairments⁷⁹. This study found that the brains of individuals with DS were deficient in SNX27 and that this deficiency may be caused by an extra copy of a microRNA (miRNA) encoded by human chromosome 21 (the miRNA is produced at elevated levels and thereby decreases SNX27 expression). Consistent with the known role of SNX27 in retromer function, decreased expression of this protein in mice disrupted glutamate receptor recycling in the hippocampus and led to dendritic dysfunction. Importantly, overexpression of SNX27 rescued cognitive and other defects in animal models⁷⁹, which not only strengthens the causal link between retromer dysfunction and cognitive impairment in DS but also has important therapeutic implications.

Hereditary spastic paraplegia (HSP) is another disorder linked to retromer. HSP is caused by genetic mutations that affect upper motor neurons and is characterized by progressive lower limb spasticity and weakness. Although there are numerous mutations that cause HSP, most are unified by their effects on intracellular transport⁸⁰. One HSP-associated gene in particular encodes strumpellin⁸¹, which is a member of the WASH complex.

The third disorder linked to retromer is neuronal ceroid lipofuscinosis (NCL). NCL is a young-onset neurodegenerative disorder that is part of a larger family of lysosomal storage diseases and is caused by mutations in one of ten identified genes — nine neuronal ceroid lipofuscinosis (CLN) genes and the gene encoding cathepsin D⁸². Besides cathepsin D, for which the link to retromer has been discussed above, CLN3 seems to function in the normal trafficking of CIM6PR⁸³. However, the most direct link to retromer has been recently described for CLN5, which seems to function, at least in part, as a retromer membrane-recruiting protein⁸⁴.

Retromer as a therapeutic target

As suggested by the first study implicating retromer in AD⁷, and in several subsequent studies^71,85, increasing the levels of retromer’s cargo-recognition core enhances retromer’s transport function. Motivated by this observation and after a decade-long search⁸⁶, we identified a novel class of ‘retromer pharmacological chaperones’ that can bind and stabilize retromer’s cargo-recognition core and increase retromer levels in neurons⁶¹.

Validating the motivating hypothesis, the chaperones were found to enhance retromer function, as shown by the increased transport of APP out of endosomes and a reduction in the accumulation of APP-derived neurotoxic fragments⁶¹. Although there are numerous other pharmacological approaches for enhancing retromer function, this success provides the proof-of-principle that retromer is a tractable therapeutic target.

As retromer functions in all cells, a general concern is whether enhancing its function will have toxic adverse effects. However, studies have found that in stark contrast to even mild retromer deficiencies, increasing retromer levels has no obvious negative consequences in yeast, neuronal cultures, flies or mice^{40, 48, 61, 71}. This might make sense because unlike drugs that, for example, function as inhibitors, simply increasing the normal flow of transport through the endosome might not be cytotoxic.

If retromer drugs are safe and can effectively enhance retromer function in the nervous system — which are still outstanding issues — there are two general indications for considering their clinical application. One rests on the idea that these agents will only be efficacious in patients who have predetermined evidence of retromer dysfunction. The most immediate example is that of individuals with PD that is caused by LRRK2 mutations. As discussed above, several ‘preclinical’ studies in flies and neuronal cultures have already established that increasing retromer levels^{71, 74}can reverse the neurotoxic effects of such mutations and, thus, if this approach is proven to be safe, LRRK2-linked PD might be an appropriate indication for clinical trials.

Alternatively, the pathophysiology of a disease might be such that retromer-enhancing drugs would be efficacious regardless of whether there is documented evidence of retromer dysfunction. AD illustrates this point. As reviewed above, current evidence suggests that retromer-enhancing drugs will, at the very least, decrease pathogenic processing of APP in neurons and enhance microglial function, even if there are no pre-existing defects in retromer.

More generally, histological studies comparing the entorhinal cortex of patients with sporadic AD to age-matched controls have documented that enlarged endosomes are a defining cellular abnormality in AD^{87, 88}. Importantly, enlarged endosomes are uniformly observed in a broad range of patients with sporadic AD, which suggests that enlarged endosomes reflect an intracellular site at which molecular aetiologies converge⁸⁷. In addition, because they are observed in early stages of the disease in regions of the brain without evidence of amyloid pathology⁸⁷, enlarged endosomes are thought to be an upstream event. Mechanistically, the most likely cause of enlarged endosomes is either too much cargo flowing into endosomes — as occurs, for example, with apolipoprotein E4 (APOE4), which has been shown to accelerate endocytosis^{89, 90} — or too little cargo flowing out, as observed in retromer dysfunction^{40, 61} and related transport defects⁵⁷. By any mechanism, retromer-enhancing drugs might correct this unifying cellular defect and might be expected to be beneficial regardless of the specific aetiology.

Conclusions

The fact that retromer defects, including those derived from bona fide genetic mutations, seem to differentially target the nervous system suggests that the nervous system is differentially dependent on retromer for its normal function. We think that this reflects the unique cellular properties of neurons and how synaptic biology heavily depends on endosomal transport and trafficking. Although plausible, future studies are required to confirm and to test the details of this hypothesis.

However, currently, it is the clinical rather than the basic neuroscience of retromer that is much better understood, with the established pathophysiological consequences of retromer dysfunction providing a mechanistic link to the disorders in which retromer has been implicated. Nevertheless, many questions remain. The two most interesting questions, which are in fact inversions of each other, relate to regional vulnerability in the nervous system. First, why does retromer dysfunction target specific neuronal populations? Second, how can retromer dysfunction cause diseases that target different regions of the nervous system? Recent evidence hints at answers to both questions, which must somehow be rooted in the functional and molecular diversity of retromer.

The type and the extent of retromer defects linked to different disorders might provide pathophysiological clues as well as reasons for differential vulnerability. As discussed, in AD there seem to be across-the-board defects in retromer, such that each module of the retromer assembly as well as multiple retromer cargos have been pathogenically implicated. By contrast, the profile of retromer defects in PD seems to be more circumscribed, involving selective disruption of the interaction between VPS35 and the WASH complex. These insights might agree with histological^{87, 88} and large-scale genetic studies⁵⁴ that suggest that endosomal dysfunction is a unifying focal point in the cellular pathogenesis of AD. In contrast, genetics and other studies⁹¹suggest that the cellular pathobiology of PD is more distributed, implicating the endosome but other organelles as well, in particular the mitochondria.

Interestingly, studies suggest that the entorhinal cortex — a region that is differentially vulnerable to AD — has unique dendritic structure and function⁹², which are highly dependent on endosomal transport. We speculate that it is the unique synaptic biology of the entorhinal cortex that can account for why it might be particularly sensitive to defects in endosomal transport in general and retromer dysfunction in particular, and for why this region is the early site of disease. Future studies are required to investigate this hypothesis, as well as to understand why the substantia nigra or other regions that are differentially vulnerable to PD would be particularly sensitive to the more circumscribed defect in retromer.

Perhaps the most important observation for clinical neuroscience is the now well-established fact that increasing levels of retromer proteins enhances retromer function and has already proved capable of reversing defects associated with AD, PD and DS in either cell culture or in animal models. The relationships between protein levels and function are not always simple, but emerging pharmaceutical technologies that selectively and safely increase protein levels are now a tractable goal in drug discovery⁹³. With the evidence mounting that retromer has a pathogenic role in two of the most common neurodegenerative diseases, we think that targeting retromer to increase its functional activity is an important goal that has strong therapeutic promise.

References

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