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What is Geriatrics?

Michael Fossel
President of Telocyte, Grand Rapids, MI 49503, USA;

E-Mail: michael.fossel@telocyte.com
OBM Geriatrics       2018, volume 2, issue 1

What is geriatrics?
All of us are intuitively aware, and many of us explicitly aware as well, of the meaning of
geriatrics as a specialty. After all, most of us practice geriatrics or we have been intimately
involved with this area and we know the reality of geriatrics. Or do we? Geriatrics is an oddly illdefined
specialty when you look at it more carefully. Some of us practice medicine, some of us
practice in the social sciences, and many of us simply do our jobs day-to-day and try to get by.
What we share, however, is the heart of geriatrics: not simply willingness, but a passion to help
others who are aging. Nor is it simply “aging” in the chronological sense, but rather it is what
happens as we age. It is what distinguishes the young newly-adult from the aging older-adult. In
keeping with this distinction, our passion is not directed at aging as chronology, but at aging as
suffering, fear, pain, disability, and the myriad other problems that arise with increasing frequency
as the years grow longer. It’s not the years, it the miles.
Geriatrics, by definition, “deals with the health and care of old people”. Caring is an essential
component of what we do, perhaps THE essential component, one all-too-often forgotten in the
day-to-day struggle of our professions, as we are squeezed for time, resources, and ability to help
those we care for. Yet, caring is not enough. The urge to help is always appreciated by those we
care for, but what of actually improving those same lives? Can we improve the health, the wellbeing,
the very function of those we care for? Can we actually improve lives in geriatrics?
Much of what we do is an uphill battle against the growing disability, disease, and risks that
accompany the aging process. We strive to control blood pressure, only to see our patients
succumb to strokes. We work hard to manage hemoglobin A1C, only to see advancing renal failure.
We encourage exercise, good diet, and stress management, only to watch as the slow creep of
Alzheimer’s disease as it erases those we care for professionally and, all too often, those we love
personally.
Too often, geriatrics becomes a holding action during a bitter retreat from a healthy life. Surely
we can do more than fight a holding action. Why not advance instead? We make the assumption
that we are all but powerless in the face of aging, that we cannot change the advance of vascular
change, the loss of joint surface, the slow evaporation of bony matrix, and the gradual failure of
memory and cognition. We think of these as not only facts of medicine, but as facts of life, as
though they are part of the very weave of reality, never to be altered.
Perhaps we are wrong.
Aging-related disease has been with human beings as long as we’ve been human. Thousands of
years ago, few of us grew old enough to suffer from the diseases we now associate with aging.
Many of us died as children, during childbirth, or from trauma, infection, and the host of diseases
that we are still prey to, long before we had the opportunity to grow old. Yet even thousands of
years ago, a few of us not only grew old, but we succumbed to age-related disease.
To take one example, Alzheimer’s disease was first named more than a century ago. Alzheimers
disease, as “Alzheimer’s” disease, was first diagnosed in about the same era that modern medicine
first began to become “modern” medicine. We have known about the shrunken brain, the amyloid
plaques, the dying neurons, and even the tau tangles for a century or so. And yet, despite the
advent of modern medicine, pharmaceuticals, and genetics, we still succumb to dementia,
Beyond Alzheimer’s and the other dementias, and again despite everything modern medicine
offers, we still succumb to a host of other age-related diseases that we lump together as aging and
that we still consign to the gentle mercies of geriatrics, and still without cures or even, some
would say, without any hope of such cures. Perhaps that hopelessness is not justified. Perhaps our
assumptions are the only thing standing between a tired hopelessness and justifiable hopes for a
better future.
That age-related disease is caused by cell aging, was first suggested twenty years ago in the
medical literature [1] and that same paper suggested that we might be able to use cell aging as a
therapeutic target. The notion that cell aging not only caused age-related diseases but could be an
effective point of intervention is consistent with everything we know about age-related disease,
everything we know about clinical medicine, and everything we know about human aging itself.
And yet, even after twenty years, we still succumb to age-related disease.
Can we do better? Can geriatrics make fundamental advances?
Age-related disease is hard for most people, even geriatricians, to understand. The key lies in
our assumptions and our fundamental understanding of how aging works at the cellular level. It is
this process that has eluded understanding, and largely due to an inability to reexamine our
premises, to examine what is really going on within aging cells. The result is that, when we deal
with age-related disease, we find that researchers, clinicians, investors, and regulatory agencies all
struggle to understand the basic pathology and to find a point of effective intervention.
The obstacle to innovative advances in geriatrics is not aging, but lies in our very assumptions
about aging. Innovation only – and always – occurs when you change your assumptions.
Most people, once they overcome their assumptions and look carefully at the diseases with a
fresh eye, realize that we not only have the ability to understand them, we have the ability to
intervene effectively. To prevent and cure age-related disease takes several things. It requires that
we understand the diseases themselves and that we have the right tools to fix the fundamental
problem. The findings that we take for the diseases themselves are, in reality, no more than
symptoms and outcomes of the diseases, rather than fundamental causes of those diseases.
Alzheimer’s is not simply amyloid plaque, vascular aging is not simply cholesterol and vessel
narrowing, osteoporosis is not simply a deficit in mineralization. All of these are no more than
biomarkers, symptoms, and findings; they are the culmination of processes that occur at the
cellular level and that are already known to be malleable to fundamental interventions. But to
intervene effectively takes more than an innovative and sophisticated understanding of cellular
aging. It also takes the ability to move from merely understanding to clinical trials. We need to
support fundamental, innovative therapies that demonstrate that geriatrics can truly make a
difference. We have the ability to provide care and compassion, and we now have the
understanding and the tools. We need only move to testing effective clinical interventions.
We need to take our compassion and our intellect and use them to move geriatrics from a
holding action into an advance toward better lives.
Competing Interests
The author has declared that no competing interests exist.
References
1. Fossel M. Telomerase and the aging cell: implications for human health. JAMA. 1998;



Problema da risolvere.. le soluzioni sarebbero tante, ma il Triage tradizionale prevale ancora nell’ approccio della medicina dell’ emergenza all’ anziano.  Il delirium è ancora una condizione cenerentola.

Le cadute un problema medico-legale prevalente.

Manca la fragilità come valutazione, la consapevolezza che il ricovero ospedaliero può essere seriamente dannoso all’ anziano, ecc . Prevalgono le chiacchere……e l’ ageismo. L’ abuso dell’ anziano tanto frequente pare non sia riconosciuto.

http://www.sigot.org/news/Il-Day-Hospital-Geriatrico—–Centro-di-Coordinamento–u-dei-servizi-per-gli-anziani–dalla-promozione-dell—invecchiamento-attivo-alla-gestione-della-fragilit—avanzata/

 

 

La SIGOT ha preso l’ iniziativa



La  sclerosi dell’ ippocampo (SH)  è un frequente riscontro autoptico nel cervello del grande vecchio ; si  associata alla demenza del grande vecchio

Circa il 10%-20%  degli ultra 85enni mostra, all’autopsia, sclerosi ippocampale, caratterizzata da perdita di cellule e gliosi ; sono interessate le zone ippocampali denominate CA1 e subiculum  (Acta Neuropathol 2013; 126: 151). Le caratteristiche neuropatologiche della sclerosi ippocampale possono essere associate a diverse cause  I dati autoptici hanno documentato che  nel 90% dei soggetti positivi alla sclerosi ippocampale era presente la proteina TDP-43, mentre solo il 9.7% di coloro che risultavano negativi alla sclerosi ippocampale presentavano TDP-43 (questa proteina si accumula anche nei neuroni motori pr esempio nella sclerosi laterale amiotrofica)  marker della malattia, accumulandosi in aggregati tossici che concorrono alla morte dei neuroni motori. Non sono stati invece individuati casi di associazione tra sclerosi ippocampale, invecchiamento e presenza dell’apolipoproteina E4. Inoltre, oltre i 95 anni di età, sembra esserci una maggiore presenza di SH, ma non di patologia dovuta dalla malattia di Alzheimer. Da questo studio è anche emerso come sia possibile determinare il profilo cognitivo di una persona, utilizzando test neuropsicologici che permettano di differenziare la SH  dal declino cognitivo conseguente a malattia di Alzheimer.   L’ arteriolosclerosi è ritenuta una possibile e probabile causa di HS ; la malattia dei piccolo vasi dovrebbe essere maggiormente considerata anche come target terapeutico (Brain 2014; 137: 255).  L’arteriolosclerosi caratterizzata dall’ispessimento concentrico delle arteriole è stata evidenziata nello studio NUN Study ; non si associa agli infarti lacunari e ad angiopatia amiloide. Gli individui con sclerosi ippocampale da invecchiamento non hanno mostrato un aumento dei tassi di ipertensione clinicamente documentata, diabete o altri fattori di rischio cardiaco.  La presenza di arteriolosclerosi  nella corteccia frontale (area Brodmann 9) si associa a SH da invecchiamento  ( p<0.001). Nella corteccia frontale dei casi con SH  da invecchiamento  le arteriole muscolari lisce actina-immunoreattivo presentano pareti più spesse ( P <0.05), perimetri di grandi dimensioni ( P <0.03), e le aree dei vasi più grandi ( P <0,03) rispetto ai controlli. A differenza delle arteriole, capillari CD34-immunoreattivo ha dimensioni che sono invariate nei casi con sclerosi ippocampale da invecchiamento rispetto ai controlli. L’arteriolosclerosi sembra essere specifica per la sclerosi ippocampale da invecchiamento del cervello; i cervelli di persone con malattia di Alzheimer non hanno mostrato le stesse alterazioni morfologiche. Un ruolo potrebbe essere svolto dai valori della pressione arteriosa nel tempo.

 

La SH da invecchiamento ha pertanto una base anatomopatologia particolare e specifica che dovrà essere oggetto di maggiori attenzioni clinico-terapeutiche. Non si deve dimenticare che la sclerosi ippocampale è presente anche in altre condizioni come l’epilessia e la sclerosi multipla.

 

 



Una raccolta fondamentale per affrontare anche da un punto di vista educativo il problema della salute mentale.

Il cervello invecchia,  la neurogenesi si mantiene, ma il microenvironment si modifica spesso in modo sfavorevole, l’ apporto ematico al cervello è spesso alterato anche per patologia delle piccole arterie e alterazioni del microcircolo

 

vedi:   https://www.nia.nih.gov/health/brain-health-resource?utm_source=20180423_BHR&utm_medium=email&utm_campaign=ealert#powerpoint

 

 



Dedication to serving the interest of the patient is at the heart of medicine’s contract with society. When physicians are well, they are best able to meaningfully connect with and care for patients. However, challenges to physician well-being are widespread, with problems such as dissatisfaction, symptoms of burnout, relatively high rates of depression, and increased suicide risk affecting physicians from premedical training through their professional careers.

These problems are associated with suboptimal patient care, lower patient satisfaction, decreased access to care, and increased health care costs.

 

da  JAMA   2018



E’ stata fatta un’indagine sulla prevalenza dell’ ansia e della depressione negli studenti del corso di laurea di Meicina e Chirurgia dell’ Università di Modena e Reggio Emilia.

I risultati sono rilevanti e meritano considerazioni e provvedimenti.

 

Ecco la presentazione : https://vimeo.com/264979437

 

Alcune Università propongono interventi preventivi  https://healthblog.uofmhealth.org/health-management/6-tools-to-help-fight-college-freshman-depression ;

Esistono certi problemi abitativi e di rapporti interpersonali che non sono per ora affrontati.

 

 



La neurogenesi  è presente a tuttte le età : la dimostrazione alla Columbia University

L’ ippocampo produce circa 700 nuovi neuroni ogni giorno.

Vedi :  https://scienze.fanpage.it/il-cervello-non-invecchia-continua-a-creare-neuroni-anche-negli-anziani

Altre ricerche recenti parlano di neurogenesi che cessa nell’ ippocampo all’ età di 13 anni.

 

L’ ippocampo concorre alla formazione dei ricordi e gestisce le emozioni. Lo striato è invece un’area associata ai sistemi della ricompensa (reward) e delle meotivazioni.

 

 


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